#10 Complications of Diabetes Mellitus

[diabetes-health-corner]

10 Complications of Diabetes Mellitus

Diabetes is a metabolic disorder, caused by the body’s inability to use the insulin produced by its own pancreas or insufficient insulin production. As glucose begins to accumulate in the bloodstream, it begins to damage the blood vessels in organs large and small across the body.

Read more how to Reduce Complication of Diabetes: https://www.freedomfromdiabetes.org/blog/post/10-complications-of-diabetes-mellitus/2713

[covid-safer-hotties]

The Long-term Complications of Covid-19 Infection - Published Sept 13, 2024

Context.— As the Covid-19 pandemic continues into its 4th year, reports of long-term morbidity and mortality are now attracting attention. Recent studies suggest that Covid-19 survivors are at increased risk of common illnesses, such as myocardial infarction, diabetes mellitus and autoimmune disorders. Mortality may also be increased. This article will review the evidence that supports some of these observations and provide an opinion about their validity and their relevance to insured cohorts.

Background Many Covid-19 survivors report protracted symptoms, sometimes lasting 3 years or more. These are collectively called post-acute sequelae of SARS-CoV-2 infection (PASC) or long Covid. They have been frequently described.1–4 In the past year, reports of long-term complications such as atrial fibrillation, heart failure, stroke and pulmonary embolism have emerged. In some reports these established disease entities are erroneously described as long Covid, generating confusion. The distinction is important: illness reported in Covid survivors are not restricted to the long Covid cohort. Thus, they are relevant to the majority of the North American population who have been infected by SARS-CoV-2, and not just the estimated 5-10% of individuals who belong to the long Covid cohort. This paper will examine the reports of increased incidence of cardiovascular diseases in both and will examine the reported long-term increase in mortality.

Cardiovascular disease after 1 and 2 years Multiple studies have reported an increased risk of cardiovascular events at 1 year. A February 2022 analysis of 153,760 US veterans, followed for 1 year after Covid-19 infection, reported an increased risk of cerebrovascular disease (HR 1.53), ischemic heart disease (HR 1.66), thromboembolic disease (HR 2.39) and atrial fibrillation (HR 1.71).5 Risk was greatest in those hospitalized and those with pre-morbid illnesses. However, risk was also elevated in outpatients, who constituted the vast majority of the cohort. These findings have been corroborated in 2 further studies. In a 2023 analysis of 690,000 Covid-19 survivors, drawn from the TriNetX database–self-described as the world’s largest global Covid-19 dataset–there was an increased risk of cerebrovascular disease (HR 1.6), ischemic heart disease (HR 2.8), thromboembolic disease (HR 2.6) and atrial fibrillation (HR 2.4) at 1 year.6 In contrast to the VA study which examined a predominantly older male population, the subjects in this study were younger, with mean age 44, and 57% were female. Risk was higher in the >65 age group and was not limited to inpatients. In a May 2023 Lancet retrospective analysis of 535,000 Hong Kong (HK) and 16,000 UK Covid 19 survivors, similar hazard ratios were recorded for stroke (HR 1.2), ischemic heart disease (HR 1.32), atrial fibrillation (HR 1.31) and deep venous thrombosis (HR 1.74).7 However, it is worth noting that while follow-up was described as 28 months for the HK cohort and 17 months for the UK cohort, the median follow-up for the HK group was 146 days and was 243 days for the UK cohort, somewhat limiting the conclusions of true impact at 1 year. Contradicting these studies, a prospective analysis of 17,000 Covid-19 survivors in the UK Biobank, did not document an increased risk of cardiovascular outcomes amongst outpatients, with the exception of thromboembolic disease (HR 2.7).8 An August 2023 analysis of 138,000 VA Covid-19 survivors followed for 2 years– the longest follow-up period to date– reported that the risk of complications in outpatients had returned to baseline at 6 months.9 In contrast, the risk for multiple cardiovascular and thromboembolic complications in the hospitalized cohort remained elevated at 2 years. None of these 5 studies was limited to individuals with long Covid, but similar findings have been reported in this group: a recent analysis of 13,435 individuals who had been diagnosed with long Covid, based on a typical array of symptoms, reported increased risks at 1 year for ischemic heart disease (HR 1.7), ischemic stroke (HR 2.1) and pulmonary embolism (HR 3.6).10

These studies document a fairly consistent, increased risk of cardiovascular complications among Covid-19 survivors. However, important questions remain. Amongst these: does increasing population immunity and vaccination change the risk? Is the magnitude of risk similar for all SARS CoV-2 variants? Does reinfection increase the risk? Answers to some are available. Vaccination appears to attenuate the risk: a Korean study of 592,000 individuals post-Covid-19 infection, showed that vaccination decreased the risk of heart attack and stroke by approximately 50%.11 This finding was replicated in a large US cohort where major adverse cardiovascular events were reduced by a similar amount for full vaccination, and by 25% for partial vaccination.12 Thus, while vaccination does not eliminate long-term complications, it appears to provide a substantial protective effect.

Reinfection may increase the risk of sequelae. In a large US VA cohort of 440,000 Covid survivors, of whom 40,000 had one or more SARS-CoV-2 reinfections, the risk of cardiovascular disorders was increased (HR 3.02), when compared to a single infection.13 Moreover, this risk was not modified by vaccination.

The impact of different variants is less clear. Most of the described studies were conducted in 2020-2021 when delta and pre-delta variants predominated. It is unclear whether similar outcomes would characterize infection with Omicron variants, which remain dominant in most countries since November 2021. Interestingly, the risk of cardiovascular complications in the cohort of Hong Kong survivors described above, where the Omicron was the prevalent strain, was no different than among the comparator UK Biobank cohort, where pre-Omicron strains were prevalent.7

Is there extra long-term mortality after Covid-19 infection? Extra mortality has been reported by several studies.6,8,14–18 A 2021 US analysis of 400 Covid-19 survivors, documented increased mortality (HR 2.5) at 1 year.14 The additional risk was confined to individuals who had been hospitalized. In 2022, 3 studies reported excess mortality in 3 different countries. The first, an Estonian whole-population study of 66,000 Covid-19 survivors, of whom 8% were hospitalized, reported a 3-fold increase in mortality at 12 months.15 Mortality was particularly elevated in the first 5 weeks following infection. For those over age 60, increased mortality persisted until 12 months (HR 2.8). However, for those less than age 60, mortality was not increased after 35 days. The second, an analysis of 690,000 Covid-19 survivors from the TriNetX database also reported increased 1-year mortality risk (HR 1.6).6 This was largely explained by excess deaths in individuals over age 65; below age 45 risk was not increased. For the outpatient cohort the risk of mortality was lower than that of the comparison group (HR 0.46). The third, a study of 25,000 Covid-19 survivors drawn from the UK Biobank, reported increased mortality risk at 20 months, for those with severe Covid infection (HR 14.7), but also an increased risk for those with mild disease (HR 1.23).16 Stratification by age was not provided.

In 2023 4 further studies reported similar, but at times quantitatively different results. Two analyses drew on the UK Biobank cohort. In the first, a prospective evaluation of 7,800 SARS-CoV-2 PCR positive individuals, increased mortality was reported for the study group at 18 months (HR 5.0), when compared to both a contemporary and an historical cohort.17 For the non-severe cases the mortality risk remained elevated (HR 4.8). The second study, already described above– a comparative analysis of 7600 Covid survivors from the UK Biobank and 530,000 Covid survivors in Hong Kong–reported increased mortality (HR 4.16) after 17 months for the former and 28 months for the latter.7 The risk of mortality was higher in the UK than the HK cohort, a difference the authors posited was due to Omicron being the dominant variant in HK during the study period. The risk remained elevated, but less so, for younger cohorts and for mild Covid-19 infections.

Finally, 2 large US studies recently reported mortality at 2 years. In the first, an analysis of 138,000 US veteran Covid-19 survivors with 5.9 million controls, the risk of death for the hospitalized cohort remained elevated at 2 years (HR 1.29).8 In contrast, the risk of death for the outpatient cohort returned to baseline at 6 months. Breakdown of risk by age-group was not provided. The second study, also of US veterans, reported similar findings. In a cohort of 280,000 Covid-19 survivors the risk of death remained elevated at 2 years (HR 2.0).18 The risk was highest in the first 90 days (HR 6.3) and decreased at 6 months (HR 1.18). Thereafter, the risk in Covid-19 survivors was slightly less than the control group (HR 0.89). A post-hoc subgroup analysis examined and refuted the possibility that accelerated mortality in the control group could have explained the lower mortality in Covid-19 survivors. The risk of death in hospitalized individuals remained elevated at 2 years (HR 1.22).

How Plausible is this Information? The studies described above command attention by virtue of their size and the consistency of their findings in different populations, and in different countries. They are also supported by the observations of long-term pathophysiologic abnormalities following SARS-CoV-2 infection, such as ongoing inflammation, persistence of virus, and immune system dysfunction. However, the negative ledger is also substantial. Observational studies such as these, no matter how well-designed, remain open to many types of bias. Reliance on diagnostic codes, prescription records, laboratory results and tallies of clinical visits, to establish disease incidence, is intrinsically error-prone and makes cross-study comparisons difficult. Perhaps more importantly, the cohorts described above were different in many respects, varying from the older, male-predominant cohort of the US VA system to the younger healthier cohort of the UK Biobank. Further, cohorts were constituted during the first year of the pandemic, at a time when healthcare delivery was disrupted, lockdowns were in effect, vaccination and antivirals were largely unavailable, and population immunity levels were low. Thus, it could be argued that the observed outcomes are better explained by an evolving pandemic, rather than solely SARS-CoV-2 infection. This could also explain the most recent reports that after 2 years of follow-up, the risk of both Covid-19 complications and mortality, in most of those infected (i.e., the non-hospitalized), is no longer elevated. It also evident that most of the reported extra mortality is occurring in the early months following infection, where survival curves separate rapidly.6,10,15,18

Are these findings relevant to an insured population? ‘Partially’ is probably the best answer. The most important observation is that hospitalization, and in-particular an intensive care unit admission, is the dominant risk factor for both morbidity and mortality. This risk appears to persist up to 2 years. The second important risk element is the presence of comorbid conditions. This observation raises the interesting question of what exactly causes the extra mortality. Is it due to ‘protracted’ SARS-Co-V-2 infection or is it caused by a recognized complication of Covid-19, such as pulmonary fibrosis or acute kidney injury? Or is it explained by an aggravation of a comorbid illness? Or is it a complication of long Covid? There is a likelihood that all these mechanisms were at play in the cohorts under study.

For non-hospitalized individuals, and those that are healthy, the evidence for extra morbidity and mortality after the first 3-6 months is far from conclusive. For the long Covid cohort, the evidence for additional mortality requires further supporting evidence. As the prevalence of co-morbid conditions is lower in insured populations, one might reasonably expect, based on current evidence, that longer-term morbidity and mortality due to Covid-19 infection will be minimally affected.

References 1.Davis H, McCorkell L, Vogel, J. et al Long COVID: major findings, mechanisms and recommendations. Nat Rev Microbiol 21, 133–146 (2023). doi.org/10.1038/s41579-022-00846-2

2.Meagher T. Long COVID - An Early Perspective. J Insur Med. 2021 Jan 1;49(1):19–23. doi: 10.17849/insm-49-1-1-5.1. PMID: 33784738.

3.Meagher T. Long COVID – One year On. J Insur Med. 2022 Jan 1;49:1–6. doi: 10.17849/insm-49-3-1-6.1. PMID: 33561352.

4.Meagher T. Long Covid - Into the Third Year. J Insur Med 2023;50(1):54–58. doi.org/10.17849/insm-50-1-54-58.1

5.Xie Y, Xu E, Bowe B et al Long-term cardiovascular outcomes of COVID-19. Nat Med 28, 583–590 (2022). doi.org/10.1038/s41591-022-01689-3

6.Wang W, Wang CY, Wang SI et al Long-term cardiovascular outcomes in COVID-19 survivors among non-vaccinated population: A retrospective cohort study from the TriNetX US collaborative networks. eClinicalMedicine. 2022 Nov;53:101619. doi: 10.1016/j.eclinm.2022.101619

7.Lam I, Wong C, Zhang, R et al Long-term post-acute sequelae of COVID-19 infection: a retrospective, multi-database cohort study in Hong Kong and the UK. eClinicalMedicine Vol. 60 Published: May 11, 2023. doi: doi.org/10.1016/j.eclinm.2023.102000

8.Raisi-Estabragh Z, Cooper J, Salih A, et al Cardiovascular disease and mortality sequelae of COVID-19 in the UK Biobank Heart 2023;109:119–126.

9.Bowe, B., Xie, Y. & Al-Aly, Z. Postacute sequelae of COVID-19 at 2 years. Nat Med 29, 2347–2357 (2023). doi.org/10.1038/s41591-023-02521-2

10.DeVries A, Shambhu S, Sloop S et al One-Year Adverse Outcomes Among US Adults With Post–COVID-19 Condition vs Those Without COVID-19 in a Large Commercial Insurance Database. JAMA Health Forum. 2023;4(3):e230010. doi:10.1001/jamahealthforum.2023.0010

11.Kim Y, Huh K, Park Y et al Association Between Vaccination and Acute Myocardial Infarction and Ischemic Stroke After COVID-19 Infection. JAMA. 2022;328(9):887–889. doi:10.1001/jama.2022.12992

12.Jiang J, Chan L, Kauffman J, et al Impact of Vaccination on Major Adverse Cardiovascular Events in Patients With COVID-19 Infection. J Am Coll Cardiol. 2023 Mar, 81(9):928–930. doi.org/10.1016/j.jacc.2022.12.006

13.Bowe B, Xie, Y, Al-Aly Z. Acute and postacute sequelae associated with SARS-CoV-2 reinfection. Nat Med 28, 2398–2405 (2022). doi.org/10.1038/s41591-022-02051-3

14.Mainous AG, Rooks BJ, Wu, et al COVID-19 post-acute sequelae among adults: 12 month mortality risk. Front Med (Lausanne). 2021;8:778434. doi:10.3389/fmed.2021.778434

15.Uuskula A, Jurgenson T, Pisarev H et al Long-term mortality following SARS-CoV-2 infection: A national cohort study from Estonia. The Lancet Regional Health - Europe 2022;18:100394 Published online 29 April 2022. doi.org/10.1016/j.lanepe.2022.100394

16.Xiang Y, Zhang R, Qiu G. et al Association of Covid-19 with risks of hospitalization and mortality from other disorders post-infection: A study of the UK Biobank. medRxiv doi: doi.org/10.1101/2022.03.23.22272811

17.Wan E, Mathur S, Zhang R et al Association of COVID-19 with short- and long-term risk of cardiovascular disease and mortality: a prospective cohort in UK Biobank, Cardiovascular Research, Volume 119, Issue 8, June 2023, 1718–1727. doi.org/10.1093/cvr/cvac195

18.Iwashyna TJ, Seelye S, Berkowitz TS, et al Late Mortality After COVID-19 Infection Among US Veterans vs Risk-Matched Comparators: A 2-Year Cohort Analysis. JAMA Intern Med. Published online August 21, 2023. doi:10.1001/jamainternmed.2023.3587

[jcsmicasereports]

Decreased erythrocyte glyoxalase 1 (GLO1) activity in patients with diabetes with reduced estimated glomerular filtration rate by Dr. Mohsen Kerkeni in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract

Background: The glyoxalase enzymes are located in the cytosol of all cells, including erythrocytes, and prevent advanced glycation end products (AGEs) production through the detoxification of the methylglyoxal (MGO). The present study was made to evaluate the GLO1 activity in diabetic patients and it relationship with estimated glomerular filtration rate (eGFR).

Patients and methods: GLO1 activity was measured spectrophotometrically in erythrocytes of 123 participants: 35 healthy subjects and 88 patients with diabetes. Biochemical parameters were measured and eGFR was calculated using the MDRD (Modification of Diet in Renal Disease) formula.

Results: We found no difference in GLO1 activity in patients with diabetes compared to healthy subjects. However GLO1 activity tended to be reduced in diabetic patients with loss renal function. A significant decrease was shown in patients with moderate to severe loss renal function. GLO1 activity was correlated with eGFR, creatinine and urea. Multivariate analysis showed that GLO1 activity was independently associated with eGFR.

Conclusion: GLO1 activity was related with loss renal function in patients with diabetes according glomerular filtration rate.

Keywords: glyoxalase 1, diabetes mellitus, glomerular filtration rate

Introduction

Diabetes is the most important disease in the wild words including type 1 diabetes, type 2 diabetes as known as diabetes mellitus (DM), and gestational diabetes [1-3]. DM is defined by chronic hyperglycemia and affected sugars metabolism caused by impaired insulin secretion [4]. Overweight and obesity are two risk factors or metabolic syndrome for developing DM. Indeed, obesity is characterized by excess body fat which is harmful to health, thus generating significant oxidative stress than chronic inflammation [5]. DM, as chronic hyperglycemia, promotes protein glycation and leads to the formation of advanced glycation end products (AGEs).

AGEs are formed by prolonged duration of hyperglycemia in diabetics and they have long-term toxicity in the body. Indeed, AGEs come from the attachment of sugar to a protein, an amino acid, or a lipid. These toxic products accumulate in all the organs leading to the activation of its RAGE receptors. A high number of publications have reported the AGEs involvement in the development of diabetes complications such as nephropathy, retinopathy, and atherosclerosis [6-8]. These products are not only present, but they also contribute to the severity of the pathology [9, 10]. The pathophysiological mechanisms of the increase in these products are still unidentified, but the formation of these products is done through the precursors of AGEs, also known as highly reactive dicarbonyl stress, the α-oxoaldehydes, such as the methylglyoxal (MGO) has a key role in detrimental effects on cellular function and has a key factor in vascular complications leading to oxidative stress. MGO is metabolized to lactate or acetol [11]. The MGO was detoxified by the glyoxalase system [12]. The glyoxalase system has two enzymes, glyoxalase 1 (EC 4.4.1.5, S-D-lactoylglutathione lyase; GLO1) and glyoxalase 2 (EC 3.1.2.6, D-hydroxyacylglutathione hydrolase; GLO2) [12]. Reduced glutathione is an essential cofactor. GLO1 catalyzes the conversion of the hemithioacetal to the thioester S-D-lactoylglutathione. The GLO2 enzyme catalyzes the hydrolysis of S-D-lactoylglutathione to form the lactate. Reduced glutathione is important for the detoxification of reactive dicarbonyls, especially methylglyoxal [13]. Therefore, we aimed to go deeper in the relation between renal function impairment and the MGO system in patients with type 2 diabetes. So, we measured the enzyme activity of glyoxalase 1 in patients with diabetes according their renal function using estimated glomerular filtration rate.

Materials and Methods

Study population

In a cross-sectional study, we recruited 123 participants (88 with type 2 diabetes) between 2019 and 2021 from CHU Taher Sfar in Mahdia-Tunisia. Data included age, weight, and height, history of diseases, smoking, and alcohol consumption. Patients were asked if they used any medication, and blood was taken. Plasma and erythrocytes cells were stored at -80°C. This study was approved by the ethics committee.

Assessments of biochemical parameters

All the analyzes of the biochemical parameters were carried out in the biochemistry department of the CHU Taher Sfar of Mahdia, These parameters were measured directly after collecting blood samples using enzymatic kits. Estimated glomerular filtration rate (eGFR) was calculated by the MDRD (Modification of Diet in Renal Disease) formula.

Measurement of GLO1 activity

GLO1 activity was measured according to Thornalley et al. [14]. Briefly, hemithioacetal was produced by incubation of MG (20mM) and GSH (20mM) for 30 minutes in an appropriate volume of sodium phosphate buffer (100mM, pH 6.6) at 37°C. The GLO1 activity was calculated and was expressed in Units/mL. One unit was defined as the amount of enzyme that catalyzes the formation of 1 µmol of S-D lactoylglutathione/min under the mentioned assay conditions.

Statistical analysis

Statistical analyzes are carried out by SPSS analysis software. Data were given as mean or median in the case of non-normally distributed data. Group comparisons were performed using the Student’s t-test or Mann-Whitney test, and the correlation coefficient was estimated using the Pearson or Spearman rank-order correlation analysis. Multivariate analysis was performed, and subgroups comparisons were performed by ANOVA test.  A P-value < 0.05 was used.

Results

Clinical parameters and GLO1 activity between healthy and diabetic subjects

Clinical parameters and GLO1 activity are shown in Table 1. Patients with diabetes had duration of diabetes between 5 and 17 years and had a high body mass index (BMI) which indicates moderate obesity in most patients. Patients with diabetes showed 48% of hypertension, and 31% of hyperlipidemia. In addition, a significant decrease of renal function, including serum creatinine and eGFR, was shown in patients with diabetes. However, GLO1 activity did not differ between the healthy subjects and patients with diabetes.

Biochemical parameters and GLO1 activity according the loss of renal function

Clinical parameters and GLO1 activity in patients subgroups according eGFR were shown in Table 2 and Figure 1. Patients with diabetes were classified in four subgroup as normal, mild, mild to moderate, and, moderate to severe according eGFR. Duration of diabetes, glucose, and HbA1c did not differ between subgroups. As expected, eGFR was deceased from normal to severe subgroups (P < 0.001). For the GLO1 activity there was no difference between normal and mild group, however, a significant decrease was observed between mild to severe subgroups (P < 0.001).

Data are shown as the mean (SD) or median (range), or number (percentage). **Significantly decreased between each group; P < 0.001 * Significantly decreased between Mild to severe group; P < 0.001

Correlation of GLO1 activity with eGFR and other variables

The GLO1 activity was correlated to eGFR (r = 0.257; P = 0.015) as shown in Figure 2. GLO1 activity was also correlated with serum creatinine (r= -0.328, p=0.002) and urea      (r = - 0.300, P = 0.020,). Multivariate analysis showed that GLO1 activity was independently associated with eGFR (b = 0.129, P = 0.038). However, GLO1 activity did not shown any correlation with glucose, HbA1c, cholesterol, and triglyceride.

Discussion

In this study, we examined the activity of GLO1 in patients with diabetes having normal to severe loss of renal function. According to our results, the GLO1 activity profile did not show a significant difference in healthy and patients. The GLO1 activity tended to be decreased with loss of renal function. We found a reduction of GLO1 activity in mild to severe loss of renal function, and was independently correlated to eGFR.

Most studies showed the role of AGEs and their interaction with their receptors, but there are a few studies about the relationships between glyoxalase system, as a antiglycation, and the loss of renal function. The first old study was done by Thornally et al. showed no significant difference in the glyoxalase enzymes between patients with dibetes and controls. However, Thornally et al. showed an increase of methylglyoxal and S-D-lactolglutathione in diabetic patients vs. controls [14]. Data concerning erythrocytes GLO1 activity in diabetes and diabetes complications are relatively scarce, and the results are controversial. Hamoudane et al. showed significantly lower GLO1 activity and glutathione levels in diabetic patients compared to controls. The levels of GLO1 activity were markedly lower in patients with diabetic complications, especially in diabetic patients with nephropathy [15]. In a study by Pacal et al. GLO1 activity was significantly increased in diabetic patients compared to controls, and was higher in nephropathy patients in stages 1-2, and remained decreased in nephropathy patients in stages 3-4 [16].  Our present study confirms the findings of Thornally et al. [14], Pacal et al. [16], Sakhi et al. [17], and Peters et al. [18]. Furthermore, Peters et al. found that GLO1 activity was lower in atherosclerotic carotid artery lesions, and the effects observed are related to the microenvironment of the damaged tissue [18]. We hypothesize that GLO1 activity may affects also the microenvironment location in glomerular and its vascular tissues under chronic hyperglycemia that induce much production of AGEs precursors such as MGO and may inhibits GLO1 enzyme activity. This AGE accumulation has been closely associated with kidney diseases, and aging. Accumulating evidence demonstrates that the progression of renal tubular damage and tubular aging are often correlated with activation of the receptor for the AGE (RAGE)-AGE pathway or decreased activity of glyoxalase 1 [19].

To our knowledge, this is the first study showing the relationships between erythrocytes GLO1 activity and the estimated glomerular filtration rate in patients with diabetes with normal, mild, moderate and severe loss of renal function. The GLO1 activity decreased markedly with patients when they have moderate to severe loss of renal function. The direct pathogenic role of MGO/glyoxalase system in the development of diabetic nephropathy is strongly supported by animal experiments. Overexpression of GLO1 in diabetic rats reduced the production of AGEs, endothelial dysfunction, and also expression of early markers of kidney damage [20].  Interestingly, knockdown of GLO1 in nondiabetic mice induces kidney pathology very similar to diabetic nephropathy [21]. The reduced levels in GLO1 activity may result also from the deceased of glutathione levels but the most biomarker that affects GLO1 activity was the tissues accumulation of α-oxoaldehydes, especially MGO that are formed during cellular metabolic reactions [14]. Recently, it was well described in a review by Schalkwijk and Stehouwer the involvement of the MGO in many diseases [22]. Lowering the MGO levels can provide new therapeutic to reduce AGEs precursors and their accumulation [23-26]. Recent interesting studies are focused on GLO1 inducers as a new therapy [27-29].

Our study has obvious limitations. We have not measured MGO or MGO-derived AGEs due to the lack of technologies in our laboratory. Furthermore, healthy subjects and patients with moderate to severe loss of renal function subgroup showed small size samples.

In conclusion, GLO1 activity in erythrocytes was independently correlated in patients with diabetes having a decreased estimated glomerular filtration rate.

Abbreviations

AGEs: Advanced glycation end products; BMI: Body mass index; DM: Diabetes Mellitus; GLO1: glyoxalase enzyme; HTA: Hypertension; MGO: methylglyoxal

Authors’ contributions

RS, HH, and AM: determined the GLO1 activity measurement, Clinical data, and wrote the manuscript. MK, SA, and AL contributed to the design and the concept of the study. HB measured the biochemical parameters. HZ: provided blood sampling. All authors read and approved the final manuscript.

Declarations

The protocol has been approved by the ethics committees at the CHU Hospital Tahar Sfar Mahdia. All participants signed the informed consent in writing before inclusion in the study.

Competing interests

The authors declare no conflict of interest.

[transorzevarsha1]

ICD-10 code E10.9 for Type 1 diabetes mellitus without complications is a medical classification as listed by WHO under the range.

[transgreeshma]

ICD-10 code E10.9 for Type 1 diabetes mellitus without complications is a medical classification as listed by WHO under the range.

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[brookemedbil]

Opening the Secrets of Medical Billing and Coding: Essential Codes You Need to Know

Unlocking the Secrets of Medical billing and ‍Coding: essential Codes You need to ​Know

In the ever-evolving world of ⁢healthcare, medical billing ⁣and coding stand⁢ as the backbone of effective and efficient patient care. This intricate process ‌ensures that ⁤healthcare providers are compensated accurately while maintaining clear interaction about⁣ patient treatment. If your looking to unravel the complexities of medical ⁣billing and coding, you’ve‍ come to the right place. In this⁣ article, we ​will explore‌ essential codes,⁣ their⁣ importance, benefits, tips, and real-world ⁣examples.

What is Medical ​Billing and ⁢Coding?

Medical billing and coding⁤ are two distinct yet interconnected processes.‌ Understanding these terms is the⁤ first step to⁢ mastering the healthcare revenue cycle.

Medical⁢ Coding

Medical ‌coding involves transforming ‍healthcare diagnoses, procedures, medical services, and equipment into universal alphanumeric ‍codes. ⁤These codes are based on established ​coding systems:

ICD-10-CM: International Classification of Diseases, Tenth Revision, ⁢Clinical Modification.

CPT: Current Procedural Terminology.

HCPCS: Healthcare Common Procedure​ Coding System.

Medical Billing

Medical billing⁢ is‌ the process of submitting and following up on claims with health insurance companies to‌ receive payment ​for services rendered.this process includes generating bills based on the codes assigned during medical coding.

Essential Codes You Need to Know

Familiarity with essential codes is ⁣crucial for anyone involved in medical billing‍ and ⁢coding. Here’s a look at some key codes you⁤ should know:

Code Type

Example Code

Description

ICD-10-CM

E11.9

type 2 diabetes mellitus without complications.

CPT

99213

Established ​patient office or other outpatient visit,level⁢ 3.

HCPCS

A4590

Miscellaneous DME supply.

Benefits of Mastering Medical Billing and​ Coding

⁣ ​ Mastering medical billing ​and coding comes with‍ numerous advantages, including:

Enhanced Efficiency: ⁣ Streamlined billing processes‌ reduce ‍administrative errors.

Increased Revenue: Proper‍ coding leads to timely ​and accurate reimbursements.

Compliance: ⁤Adhering to coding standards helps⁣ avoid legal‍ issues ​and penalties.

Practical Tips for Success in Medical ‌Billing and Coding

​ ‍ ⁢ ‍ ​ Implementing effective‌ strategies can⁢ enhance your ‌skills in medical billing and ⁣coding. Here ​are some practical tips:

Stay Updated

The‍ world of medical coding‌ is constantly changing. Subscribe to industry newsletters and official bodies to keep up.

Invest in quality Training

Consider ⁣enrolling in accredited courses to gain a solid ‍foundation in coding practices.

Practice Adequate⁣ Record-Keeping

Maintain organized records of‌ all claims,​ payments, and denials ‍for easy reference.

Real-World Case ​Study

Increasing Revenue Through Accurate Coding

A small clinic struggled with low reimbursement rates due to frequent coding errors.⁢ After ⁢hiring‌ a ⁣certified medical coder,they saw a 30% increase in revenue over six months. By ensuring ‌that every service ⁤was appropriately⁤ coded using⁤ accurate ICD-10-CM and CPT codes, the⁤ clinic‌ maximized its claim potential.

First-Hand ⁣Experience:​ Insights ⁣from ‌Professionals

Manny professionals share their experiences about the importance of detailed coding:

“Having a clear understanding of medical ‍terminologies and ⁤coding systems ⁣is crucial. It not just increases the⁣ chances of getting paid;​ it also​ helps ⁣in understanding the​ patient’s journey through the healthcare​ system.” – John Doe, Certified Medical Coder

Conclusion

Understanding medical billing and coding is vital in today’s healthcare landscape. ⁣By familiarizing yourself with essential codes, embracing ‍best practices, ⁤and learning from case studies, you ⁣can enhance your skills in this critical field. Remember, correctness ‌in coding ‌translates into efficiency in‍ billing, which ultimately affects the financial ⁣health of healthcare providers. Unlock the secrets of medical billing and⁤ coding, and join this rewarding journey in⁢ healthcare finance.

https://medicalbillingcodingcourses.net/opening-the-secrets-of-medical-billing-and-coding-essential-codes-you-need-to-know/

[sahraeyll]

Decoding Medical Billing: A Comprehensive Guide to the World of Healthcare Coding

**Title: Decoding Medical Billing: A Comprehensive Guide to​ the World of Healthcare ⁣Coding**

**Introduction:** In the complex world of healthcare, medical billing and coding​ play⁢ a vital⁣ role in ensuring accurate and ⁣efficient processing of‌ medical claims.⁢ Understanding the ins and outs of medical billing can be daunting,⁤ but fear not! In this comprehensive⁣ guide,⁣ we will break down ​the ⁢basics of medical‌ billing and coding, explain the importance⁤ of⁢ accurate coding, and provide practical tips for success in ⁢the world of ​healthcare coding.

**The Importance of Medical Billing and Coding:** Medical ‌billing and coding are essential processes in the healthcare industry‍ that ​help translate medical services into universal codes for insurance​ reimbursement. Accurate coding ​ensures that healthcare providers receive‌ proper payment for their services and that patients ⁢are billed ‌correctly. In addition,​ coding helps maintain accurate patient records, facilitate research, and ensure compliance ⁢with regulatory requirements.

**Benefits of Proper Medical Billing and Coding:** – Ensures ⁣accurate reimbursement ​for healthcare services – Reduces billing errors ‍and‌ claim denials – Improves efficiency in healthcare operations -‍ Facilitates accurate patient records and research – Ensures compliance with coding and⁢ billing ‍regulations

**The Basics of ‍Medical Coding:** Medical coding involves assigning alphanumeric codes to medical diagnoses, procedures, and‌ services. There are two main code sets used in medical coding: ICD-10-CM (International Classification of Diseases,⁢ 10th Revision, Clinical Modification) and CPT ⁢(Current Procedural Terminology). ICD-10-CM codes are⁤ used ⁤to describe diagnoses, while CPT ‍codes are used to describe medical⁢ services and procedures.

**Code Examples:** Below are some examples of ICD-10-CM and CPT codes:

| ICD-10-CM Code‍ ⁣ | Description ​ ⁢ ⁢ ​ ⁤ | |———————–|———————————————————-| | J40.1 ⁢ ‍ | Acute exacerbation of simple chronic bronchitis⁢ ​ | | ⁢E11.9 ⁣ ‍ ​ ‍ | Type 2 diabetes​ mellitus without complications |

| CPT Code ‍ |‌ Description ⁣ ‌ ‍ ⁣ ‌ | |———————-|———————————————————–| |​ 99213 ​ ⁤ ⁢ | Office or other outpatient visit ​for the evaluation and management of an established patient |

**The Role of Medical Billers and Coders:** Medical billers and ‌coders are trained professionals responsible for​ interpreting medical records, assigning appropriate codes, and ‌submitting claims to insurance companies for reimbursement. They must​ be ⁤detail-oriented, well-versed in coding guidelines, and knowledgeable about⁢ insurance policies and regulations.

**Practical Tips for Medical Billers and Coders:** -⁢ Stay updated on coding guidelines ⁤and regulations – Double-check codes for accuracy – Communicate effectively with⁣ healthcare providers​ and insurance ⁢companies – Keep detailed documentation of all coding activities – Seek continuing education and certification opportunities

**Case Study:** Sarah is a medical coder working at a busy healthcare facility. She recently encountered a complex medical case ​involving multiple⁤ procedures and diagnoses. ⁢By carefully reviewing the medical records, consulting coding guidelines, and ​seeking clarification from the healthcare provider, Sarah was able to ‍accurately code the case and submit a ⁢successful claim for reimbursement.

**Conclusion:** Medical billing‌ and ‌coding ​are crucial components of the healthcare system that ensure accurate reimbursement, improve efficiency, and maintain compliance with coding ‌regulations. By understanding the‌ basics of medical coding, staying updated on coding guidelines,‌ and following ​best practices, medical billers and coders can navigate the complexities of healthcare coding with confidence. With the right knowledge and skills, you can decode the world of‍ medical billing and coding like a pro!

https://medicalbillingcertificationprograms.org/decoding-medical-billing-a-comprehensive-guide-to-the-world-of-healthcare-coding/

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Cold

Symptoms – sore throat, sneezing, runny/blocked nose, cough, mild fever, pressure in ears, headache, myalgia (pain in muscles)

Duration – 1-2 weeks, symptoms peak 2-3 days, incubation period 10-12 hrs

Referral criteria – suspected flu, earache not responding to analgesia, sinus pain not responding to decongestants, no improvement after 10-14 days self-medication

Complications - immunocompromised, who smoke, and with comorbidities such as diabetes mellitus, congestive heart failure, asthma, chronic obstructive pulmonary disease, cystic fibrosis, and sickle-cell disease

Sinusitis – prolonged nasal congestion and facial pain

LRTI - acute bronchitis, acute exacerbation of asthma or chronic obstructive pulmonary disease (COPD), and community-acquired pneumonia

Acute otitis media – common in younger patients

Differential diagnosis

Meningitis – high fever, drowsiness, blank expression, vomiting, loss of appetite, high pitched screaming, non-blanching rash, photophobia, severe headache, malaise

Upper airway obstruction – noisy breathing, drooling, inability to swallow.

Nasal foreign body – persistent discharge from 1 nose with no other symptoms

Management – paracetamol or ibuprofen for headache, muscle pain or fever – only continue use if distressed, change to other agent if not alleviated, don’t give both together

Paracetamol contraindicated in – liver/kidney problems, epileptic

Ibuprofen contraindicated in – pregnancy, perforated stomach, increased bleeding, severe HF, kidney or liver problems, high BP, asthma, hay fever

Intranasal decongestants – improve breathing and promote sleep and has fewer S/E than oral decongestants. Ephedrine HCL 0.5% nasal drops for 12 and older p 1-2 drops 4x daily for 1 week – contraindicated – diabetes, hypertension, hyper thyroidism, CVD, high BP, MAOI in last 2 weeks

Oral decongestants – relieve nasal congestion (phenylephrine) – max 1 week

Antitussive (cough) – dextromethorphan

Expectorants (guaifenesin)

Chlorphenamine or Beecham’s (contains phenylephrine and paracetamol) (Sedating antihistamine – dries up secretions)

Counselling points

Go to GP if

fever for more than 3 days

symptoms worsening after 5 days

symptoms not better after 10 days

follow up meeting

risk and complicated patients within the week

young children – 1 week

Headaches

Types of headaches

Primary – not associated with other conditions – migraines, tension types, cluster

Secondary – associated with other conditions – trauma/injury, vascular disorders, hyper-tension, withdrawal such as opioids, analgesics, or alcohol. Bacterial or viral infection.

Features of serious headache – referral

New severe or unexpected headache – sudden onset reaching max intensity 5 mins and new onset in over 50s

Progressive or persistent headaches that changed dramatically

Associated features – fever, impaired consciousness, seizure, stiffness, photophobia, neurological deficit, cognitive dysfunction, atypical aura (greater than 1 hour) or aura 1st time in patients using combined oral contraceptives.

Dizziness, visual disturbance, vomiting. Head trauma up to 3 months prior, triggered by coughing, sneeze, or physical exertion. Worsened by standing or lying down.

Compromised immunity

Diagnosis

Migraine without aura – at least 5 attacks lasting 4-72 hrs with unilateral location (half the face), pulsating, moderate to severe pain and aggravated by or causing avoidance of routine physical activity. Attack comes with nausea and/or vomiting, photophobia and phonophobia

Migraine with aura – 2 attacks with visual aura (zigzag lines or blind spots), pins and needles, speech/language symptoms, motor weakness, vertigo.

One aura spreading gradually for 5 mins and 2 or more occurring after

Each aura lasts for 5-60mins which is unilateral

Management – stop combined oral anticontraception – contraindicated

Ibuprofen 400mg, paracetamol 1g, advise med to be taken at start of attack – follow up 2 weeks

Tension type – recurrent episodes lasting 30 mins – 7 days with NO nausea or vomiting. May have phot/phono phobia

Bilateral (across head landscape), pressing or tight (not pulsating), mild to moderate pain, not aggravated by physical activity

Management – simple analgesia – paracetamol or NSAID

Identify comorbidities such as stress, mood disorders, chronic pain, sleep disorders to manage

Cluster headache – 5 attacks of severe/very severe unilateral orbital (around ONE eye), forehead or temporal pain lasting 15 mins to 3 hrs with nasal congestion, runny nose, eyelid oedema, sweating, facial slushing, fullness in ear or restlessness

Attacks occur between one every other day and 8 per day for more than half the time the disorder is active

Management – REFER

Advise to avoid triggers and risk of medication overuse, identify and manage comorbidities – insomnia, depression, and anxiety

Medication – occurs 15 days per month and have a pre-existing headache disorder. Regular overuse of drugs for 3 months

Management – withdrawal from medication and advice around this

Sinusitis

Sinusitis usually follows a cold and lasts less than 12 weeks

If over 12 weeks becomes chronic – risk groups are allergic rhinitis, asthma, immunosuppression

Symptoms

Adults

Nasal blockage (obstruction/congestion), nasal discharge, facial pain/pressure, frontal headache, loss, or reduction of smell, altered speech indicating nose blocked. Tenderness, swelling. Redness over cheekbone, cough, headache worse when bending or lying down. Toothache.

Children

Nose block, discoloured nasal discharge, facial pain, pressure and or cough at day or night-time

Bacterial sinusitis

More than 10 days, discoloured, pussy discharge (from 1 nose), severe local pain (1 side), fever over 38 degrees, deterioration after milder sickness

Refer to hospital immediately

If they have symptoms of acute sinusitis and;

Severe systemic infection

Intraorbital or periorbital complications, including periorbital oedema or cellulitis, displaced eyeball, double vision, or new reduced vision

Intracranial complications, including swelling over frontal bone, symptoms or signs of meningitis, severe frontal headache, or focal neurological signs

Refer to GP

Severe symptoms, painkillers don’t work, symptoms worsen, symptoms don’t improve after 1-week, recurrent infection, sudden worsening, antibiotic failure, unusual or resistant bacteria, recurrent episodes, immunocompromised, allergic cause

Treatment

Acute with symptoms less than 10 days

DON’T OFFER ANTIBIOTIC, assure that it usually self resolves without bacterial complications. Symptoms managed

Paracetamol or ibuprofen for pain, headache, and fever

Use nasal saline spray or decongestants spray

Clean nose with saltwater solution (boil 1 pint of water and add 1 teaspoon of salt and bicarbonate soda. Wash hands, stand over sink, cup the palm of 1 hand and pour small amount of solution into it. Sniff water into 1 nostril at a time, breath through mouth and allow water to pour into sink, don’t let it go into your throat. Do 3x daily)

Acute for 10 days or more with no improvement

High dose nasal corticosteroid for 2 weeks for over 12s (mometasone 200mcg 2x daily)

Counsel that It may improve symptoms but won’t make the infection any shorter, could have systemic effects, may be difficult to use correctly.

Symptoms should get better 3-5 days of treatment – REFER if not

1st line antibiotic for adult

If not life threatening - phenoxymethylpenicillin 500 mg four times a day for 5 days.

Is systemically unwell, symptoms of more serious illness or high risk of complications - co-amoxiclav 500/125 mg three times a day for 5 days.

Allergic or intolerant to penicillin - clarithromycin 500 mg twice a day for 5 days.

Pregnant or intolerant to penicillin - erythromycin 250 mg to 500 mg four times a day or

Children 1st line

Phenoxymethylpenicillin

1 to 11 months, 62.5 mg four times a day for 5 days. 

1 to 5 years, 125 mg four times a day for 5 days. 

6 to 11 years, 250 mg four times a day for 5 days. 

12 to 17 years, 500 mg four times a day for 5 days.

If very unwell - co-amoxiclav

1 to 11 months, 0.25 mL/kg of 125/31 suspension three times a day for 5 days. 

1 to 5 years, 5 mL of 125/31 suspension three times a day or 0.25 mL/ kg of 125/31 suspension three times a day for 5 days

6 to 11 years, 5 mL of 250/62 suspension three times a day or 0.15 mL/kg of 250/62 suspension three times a day for 5 days. 

12 to 17 years, 250/125 mg three times a day or 500/125 mg three times a day for 5 days.

If allergic or intolerant to penicillin – clarithromycin

Under 8 kg, 7.5 mg/kg twice a day for 5 days. 

8 to 11 kg, 62.5 mg twice a day for 5 days. 

12 to 19 kg, 125 mg twice a day for 5 days. 

20 to 29 kg, 187.5 mg twice a day for 5 days. 

30 to 40 kg, 250 mg twice a day for 5 days. 

12 to 17 years, 250 mg twice a day or 500 mg twice a day for 5 days.

2nd line – if symptoms are still worsening after 1st line treatment for 2-3 days

Adults – co-amoxiclav 500/125mg TD x 5 days

Children – specialist advice

ANTIHISTAMINES can be prescribed for allergic triggered sinusitis

Diabetes type 1

Body stops making insulin and the blood sugar (glucose) level goes extremely high - persistent hyperglycaemia (random plasma glucose of 11mmol/l or more). We must control glucose level with insulin injections, healthy diet and reduce the risk of other health complications. Typically occurs in children and young adults.

Symptoms of T1D- Frequently thirsty, pass a lot of urine, tiredness, weight loss and feeling generally unwell. Develops quite quickly, over days or weeks, as the pancreas stops making insulin.

Pathophysiology of T1D- Autoimmune disease (environmental & genetic factors). Antibodies attach to the beta cells in the pancreas destroying the cells that make insulin (pancreatic islet cells).

Diagnosing T1D- Simple dipstick test to detect glucose in a sample of urine BUT only way to confirm the diagnosis is to have a blood test to look at the level of glucose in your blood (level of 11.1 mmol/L or more in the blood sample indicates that you have diabetes) PLUS a fasting blood glucose level is taken (level of 7.0 mmol/L or more indicates that you have diabetes).

Management- Should be offered multiple daily injection basal-bolus insulin regimens as the first-line choice. Twice-daily insulin detemir should be offered as the long-acting basal insulin therapy. Once-daily insulin glargine may be prescribed if insulin detemir is not tolerated, or if a twice-daily regimen is not acceptable to the patient. Insulin detemir may also be offered as an alternative once-daily regimen. There are multiple types of insulin…

Rapid Acting- Insulin Aspart (Novorapid®), Lispro (Humalog®) and Glulisine (Apidra®)

Short Acting- Soluble insulin (Actrapid®)

Intermediate Acting- Isophane (Insulatard® or Humulin I®) & NPH - neutral protamine Hagedorn

Long Acting- Insulin glargine (Lantus®), detemir (Levemir®)

Combination insulins (biphasic)- e.g., Novomix 30®, Humalog Mix 25®, Humalog Mix 50®, Humulin M3® and Insuman Comb 50®

Diet & Lifestyle- Diet low in fat, salt, and sugar and high in fibre and with plenty of fruit and vegetables. If you are overweight try to lose weight, increase your physical activity even if it’s only going for a walk (community groups)

Other Health Complications- Get regular checks with your GP, podiatrist, and optometrist. Also get the flu jab every year.

Complications – microvascular, macrovascular (MI, stroke), metabolic (diabetic ketoacidosis) and hypoglycaemia (blood glucose less than 3.5mmol/l)

Psychological complications – anxiety, depression, and eating disorders and those at increased risk of developing autoimmune diseases

Suspect DKA in diabetics – greater than 11mmol/L

Increased thirst and urine frequency, inability to tolerate fluids, persistent vomiting, diarrhoea, visual disturbance, lethargy, fruity smell on breath, deep sighing when breathing and dehydrated

Management

HbA1c levels target of 48mmol/mol or lower - Measure 3-6 months but more often if not controlled

Self-monitoring – need glucose monitor, lancet, finger pricking device and testing strips

Taught at diagnosis and review technique 1 yearly.

Before breakfast, 2 hours after meals, during illness, before driving, if they feel hypo – at least 4 times a day including before and after meals and before bed.

More frequency required (up to 10x daily) if

Target HbA1c not achieved, frequency of hypo increases, during illness, before, during and after sports, planning, during and while breastfeeding.

Target glucose readings

Fasting plasma glucose level of 5–7 mmol/L on waking.

Plasma glucose level of 4–7 mmol/L before meals at other times of the day.

For adults who choose to test after meals, plasma glucose level of 5–9 mmol/L at least 90 minutes after eating.

Agree bedtime target plasma glucose levels with the person. This should:

Consider the timing of the last meal and its related insulin dose.

Be consistent with the recommended fasting level on waking.

Provide information of effects of food and drinks – carbohydrate training (match carb quantities to insulin doses)

Educate to be careful of body weight and diets, feasting and fasting, fibre and protein intake, diabetic foods and sweeteners, alcohol intake, matching carbs with insulin and physical activity

Advice on alcohol – avoid drinking on empty stomach, eat carb snack before and after drinking (extra insulin not required). Measure glucose more regularly and maintain it with carb intake. Alcohol can exacerbate or prolong hypoglycaemic effect.

Exercise – lower glucose levels and reduces CVD risk and can help weight

Sick day rules – never stop or skip insulin – dose may need altering seek advice. Check blood more frequently – 1-2 hours including in the night. Check blood or urine ketone levels – 3-4 hours including night and if 2+ or 3mmol/l or higher then contact GP immediately.

Maintain normal meal pattern where possible if not then replace meals with carb rich drinks, milk, fruit juices and sugary drinks. Aim to drink at least 3L of fluid to prevent dehydration.

Offer multiple daily injection basal-bolus insulin regimens as the first-line choice to all adults with type 1 diabetes.

Offer twice-daily insulin detemir as the long-acting basal insulin therapy

Offer a rapid-acting insulin analogue injected before meals for mealtime insulin replacement

If a multiple daily injection basal–bolus insulin regimen is not possible and a twice-daily mixed insulin regimen is preferred

Insulin pump therapy is recommended as a treatment option for adults with type 1 diabetes mellitus if condition isn’t controlled by treatment

Diabetes type 2

The body still makes insulin however, you do not make enough insulin for your body's needs OR the cells in your body do not use insulin properly (insulin resistance means you need more insulin than normal make to keep glucose levels down. Occurs mainly in people aged > 40 but inc diagnosed in younger people, commonly associated with obesity, physical inactivity, raised blood pressure, dyslipidaemia, and a tendency to develop thrombosis (CV risk).

Symptoms of T2D- Gradual (weeks-months) and can be quite vague at first. Frequent thirst, passing large amounts of urine, tiredness, which may be worse after meals. Some people also develop blurred vision and frequent infections, such as recurring thrush.

Management- Metformin HCl 1st choice for treatment of all patients (à weight loss, red risk of hypoglycaemic events and long-term CV benefits). Has an anti-hyperglycaemic effect, lowering both basal and postprandial blood-glucose conc. It does not stimulate insulin secretion and therefore, when given alone, does not cause hypoglycaemia. If metformin contra-indicated/not tolerated trial MR formulation or initial treatment should be a sulfonylurea e.g. gliclazide OR a dipeptidyl peptidase-4 inhibitor e.g. linagliptin OR Pioglitazone.

Insulin- can be added if intensification of treatment needed. If needed, bedtime basal insulin should be initiated, and the dose titrated against morning (fasting) glucose.

Diet & Lifestyle- Avoid foods heavy in saturated/trans fats, beef and processed meats, sugary drinks, high-fat dairy products and salty/fried foods & have fibrous fruits and vegetables, high omega-3 fatty acid food and poly/monosaturated fats. Lose weight and inc physical activity (min 5 x 30 min brisk walk / week) and smoking cessation.  Also see optician regularly in case of damage to retina, GP and podiatrist.

EXTRA INFO FOR BOTH

Holiday- Pack about x3 the amount of insulin needed, test strips, lancets, needles or glucose tablets you would use, in case you need it (take cool bag to avoid insulin getting too hot). Carry your medicine in your hand luggage just in case checked-in bags go missing or get damaged (insulin can freeze and render it unusable). If injecting (i.e. will have needles/sharps) get a letter from your GP that says you need it to treat diabetes. If you use a pump or CGM, check with your airline before you travel about taking it on board as may require paperwork for medical equipment. If you use a pump, pack insulin pens in case it stops working. Take plenty of snacks in case there are any delays. Do not put your pump through the hand luggage scanner – let airport security know so they can check it another way.

<18 & Diabetic- Paediatric diabetes care team until 18 will help w injecting insulin, testing blood glucose levels, and diet. They can give advice on school or nursery and talk to your child's teachers and carers. Initially, every 1 - 2 weeks but will eventually be every 3 months.

Check Ups Needed- Annually get feet checked by podiatrist to check for loss of feeling in your feet, and for ulcers and infections. Get your eyes checked to check for any damage to blood vessels in the eyes, and checks for high blood pressure, heart, and kidney disease by your GP, also ensure to book in annually for a flu jab. Every 3 months have a blood sugar test (HbA1C test) checks your average blood sugar levels and how close they are to normal when newly diagnosed, then every 6 months once you're stable (~48-53 mmol/mol recommended).

Education- free education courses to help you learn more about and manage your diabetes, your GP will need to refer you. Diabetes UK run local charities for extra support, their website plus the NHS website offers a lot of diabetes information and advice. Maybe invest in a medical ID to carry w you.

Extra Lifestyle Advice- Eat a meal w carbs (e.g. pasta) before you drink alcohol and make sure people around you can recognise a hypo, choose diet soft drink mixers where possible, check your blood glucose regularly/before bed/the next day, drink plenty of water the next day. Avoid hypos by eating the right amount of carbs before, during and after exercise, adjust your insulin and check your blood glucose regularly, drink plenty of water. Recommended to have HbA1c <48mmol/mol when pregnant as high blood glucose levels can harm your baby, especially in the first 8 weeks of pregnancy, also a risk of having a large baby, which can cause complications during labour. Speak to your diabetes team If you're planning to get pregnant or if you get pregnant unexpectedly.

Item for disposal

Method of disposal

Needles

Sharps bin

Lancets

Sharps bin

Used blood test strips

Sharps bin

Leftover/expired insulin

Sharps bin/return to pharmacy

DVLA- tell the DVLA you’re diabetic or you could get fined due to hypoglycaemia/low sugar levels crisis. Check your blood glucose no longer than 2 hours before driving, check your blood glucose every 2 hours if you're on a long journey, travel with sugary snacks and snacks with long-lasting carbs, like a cereal bar or banana. If you feel your levels are low: stop the car when it's safe, remove the keys from the ignition, get out of the driver's seat, check your blood glucose, and treat your hypo, don't drive for 45 minutes from when you feel normal again.

Sharps Removal- Patients issued a sharps bin from the diabetes clinic/hospital on first diagnosis. Some pharmacies offer this sharps disposal service, or the diabetes clinic do too. Can arrange w GP/LHB for sharps collection (Cardiff Council does NOT offer kerbside sharps disposal)

Other Technologies- Insulin Pump (attached to skin via tiny tube which is replaced every 2-3 days & pump moved to diff part of body) will deliver a set background amount of insulin into blood day and night, can add your extra mealtime insulin using the pump. Continuous glucose monitoring (CGMs) means you can check your sugar levels at any time (see patterns in your levels, sends an alert if glucose too high/low) but as interstitial fluid sugar readings are a few mins behind your blood sugar levels you'll still need to do finger-prick checks every now and then. It’s a sensor you attach to your abdomen which needs replacing every 7 days, but some models can be worn for months. Free Style Libre is a flash glucose monitoring system measures your glucose levels continuously throughout the day via interstitial fluid (few mins behind). Attach sensor to your arm and a reader will scan to see your sugar levels (can also use a smartphone app to scan the sensor), sensors usually last for 14 days.

Testing blood glucose

Glucose monitor, specific in-date test strips, primed lancing device and cotton wool pad.

PRIMING LANCET

Twist cap off lancing device

Place fresh lancet into device so grooves line up and twist off the cover, so the needle is visible – change lancet every time so you don't get skin infections

Replace device cap - it should click and then adjust the depth metre – how far the needle will puncture – this is personal preference

Pull sliding barrel at bottom of device back to prime the lancet

CALIBRATING MONITOR

Turn on monitor – put new in-date test strip inside it and test it with in-date control solution – to make sure readings are correct

Do this every time you open a new pack of test strips, if you damage your monitor and if you think the readings are wrong.

TESTING process

Wash hands with warm water and soap and dry. Then rub hands for 10 seconds – warms hands to improve blood flow to fingers

Turn on monitor and place strip inside and wait for it say it’s ready for blood

Place device firmly on side of the finger (less nerves so less painful) and press release button then remove device from site. - change fingers regularly to stop hardening of skin.

Wipe first drop of blood away with cotton pad, use second one to test make sure by touching the blood onto the test strip

If successful wipe blood with cotton pad and apply plaster

Note readings

Remove cap of device exposing lancet. Place lancet cover on table and press lancet hard into this blue plastic cover – this will cover the needle and make it easy to remove

Place lancet and cotton pad in bin

Injecting insulin

Inject in stomach, thighs, or buttocks. Inject an inch away from previous site. Prevents lumps – this reduces absorption of insulin.

check that its correct insulin and is in date. Always check manufacturer’s instructions.

Wash hands with soap and warm water

Attach needle to pen – peel back cover, screw cap onto pen, remove white outer cover and the green cover to expose needle – change needle every time

Dial to 2 units and push plunger so you can see insulin coming out – to make sure no air stuck in there – can take multiple goes in new pens

Set correct dose

Press directly into skin and inject slowly – count to 10 

Remove needle straight without bending it

Use the white outer cap to remove the needle and dispose in yellow sharps bin

Asthma

Symptoms – episodic, worse at night/early morning, triggered by exercise, infection and exposure to cold air or allergens. Triggered by emotion and laughter in children. In adults by NSAIDS and BB use.

Common with atopic eczema, dermatitis and allergic rhinitis and family history

ACUTE EXACERBATION OF ASTHMA IN ADULTS

First-line treatment for acute asthma is a high-dose inhaled short-acting beta2 agonist (such as salbutamol) given as soon as possible. For patients with mild to moderate acute asthma, a pressurised metered-dose inhaler and spacer can be used. For patients with acute severe or life-threatening symptoms, administration via an oxygen-driven nebuliser is recommended, if available. If the response to an initial dose of nebulised short-acting beta2 agonist is poor, consider continuous nebulisation with an appropriate nebuliser. Intravenous beta2 agonists are reserved for those patients in whom inhaled therapy cannot be used reliably.

In all cases of acute asthma, patients should be prescribed an adequate dose of oral prednisolone. Continue usual inhaled corticosteroid use during oral corticosteroid treatment. Parenteral hydrocortisone or intramuscular methylprednisolone are alternatives in patients who are unable to take oral prednisolone.

IN CHILDREN OVER 2

First-line treatment for acute asthma is an inhaled short-acting beta2 agonist (such as salbutamol) given as soon as possible. For children with mild to moderate acute asthma, a pressurised metered-dose inhaler and spacer device is the preferred option. The dose given should be individualised according to severity and adjusted based on response. For children with acute severe or life-threatening symptoms, administration via an oxygen-driven nebuliser is recommended, if available. Parents/carers of children with acute asthma at home, should seek urgent medical attention if initial symptoms are not controlled with up to 10 puffs of salbutamol via a spacer; if symptoms are severe, additional bronchodilator doses should be given as needed whilst awaiting medical attention. Urgent medical attention should also be sought if a child's symptoms return within 3-4 hours; if symptoms return within this time, a further or larger dose (maximum of 10 puffs of salbutamol via a spacer) should be given whilst awaiting medical attention.

COPD

Symptoms - persistent respiratory symptoms and airflow obstruction, which is usually progressive and not fully reversible, exertional breathlessness, chronic/recurrent cough, or regular sputum production, wheeze

Treatment – education on condition and risk factors, smoking cessation, pneumococcal and flu vaccination yearly, treatment of associated comorbidities

1st line – SABA or SAMA to relieve breathlessness and improve exercise tolerance – reviewing medication, adherence, and inhaler technique regularly

THEN IF they have NO asthmatic features or no features of steroid responsiveness – offer LABA AND LAMA

If they continue to have day-to-day symptoms, consider 3-month trial of LABA+LAMA+ICS

If NO improvement go back to LAMA+LABA only but if it works continue and review annually

If they have asthmatic or steroid responsiveness features offer LABA+ICS if they have day to day symptoms of 1 severe or 2 moderate exacerbations a year, then offer LABA+LAMA+ICS

WITH ICS DISCUSS RISK OF USING ICS including pneumonia

Acute exacerbation of COPD – triggered by infections, smoking and environmental pollutants

Severe breathlessness, increased cough, increased sputum production and change in colour, increased wheeze, and chest tightness, cold or sore throat, reduced exercise tolerance, ankle swelling, increased fatigue, and acute confusion

FOR SEVERE exacerbation – ADMISSION

FOR non-severe – increase dose or freq of SABA and maybe change to nebuliser for ease of admission

If no contraindications with significant increase in breathlessness – offer 30mg oral prednisolone OD x 5 days or if caused by infection then amoxicillin 500mg TD x 5 days, doxycycline 200mg day 1, 100mg OD x 5 days, or clarithromycin 500mg BD X 5 days

Epilepsy

Cause – abnormal excessive or synchronous brain activity

Symptoms

Short-lived (less than 1 minute), abrupt, generalised muscle stiffening with rapid recovery — suggestive of tonic seizure.

Generalised stiffening and subsequent rhythmic jerking of the limbs, urinary incontinence, tongue biting —suggestive of a generalised tonic-clonic seizure.

Behavioural arrest — indicative of absence seizure.

Sudden onset of loss of muscle tone — suggestive of atonic seizure.

Brief, 'shock-like' involuntary single or multiple jerks —suggestive of myoclonic seizure.

Management

During seizure – protect from injury by placing in recovery position. If tonic-clonic seizure is prolonged (more than 5 mins) or recurrent – emergency buccal midazolam or emergency admission

Annually reviewed – assess seizure control, how it’s affecting QOL, adverse effects and compliance with drug

Women of childbearing age – 13 to 60

Epileptic women not treated with drugs or on non-enzyme inducing antiepileptic (except lamotrigine) – contraceptive options are same as general population

Woman on exyzme-inducing drugs – drug can reduce effectiveness of combined hormonal contraception, progestogen-only pills, transdermal patches, the vaginal ring, and progestogen-only implants. OFFER medroxyprogesterone acetate injections or an intrauterine method (copper intrauterine device or the levonorgestrel-releasing intrauterine system)

Woman on lamotrigine – oestrogen containing contraceptive reduces efficacy of lamotrigine

USE progesterone only instead but educate them to report signs of lamotrigine toxicity

Category 1 (ensure the person is maintained on a specific manufacturer's product) — phenytoin, carbamazepine, phenobarbital, primidone.

S/E – common and usually mild, advise to report and can usually be fixed with dose adjustment or change of drug

Sedation and dizziness, suicidal thoughts and behaviour, acute psychotic reactions, weight gain and loss, skin rashes.

Safe in pregnancies – lamotrigine (Lamictal) and levetiracetam (Keppra) are safest options

Anxiety

Uncontrollable widespread worry and range of cognitive and behavioural symptoms

Slow onset and symptoms don’t usually improve but are better controlled with intervention

Diagnosis – worry associated with restlessness, insomnia and muscle tension, fatigue, poor concentration, irritable. ALWAYS ask about alcohol and drug use including OTC

Treatment

Establish diagnosis and severity of anxiety and any other comorbidities (usually insomnia and depression and whichever is the most pressing is treated first) – explaining the disorder and treatment opportunities and starting them with active monitoring of symptoms either self or through regular meetings

Offer CBT – non-facilitated self-help for 6 weeks, individual guided self-help, educational groups

High intensity CBT, applied relaxation or drug therapy

Drug therapy – 1st line is SSRI (sertraline, paroxetine, or escitalopram) 2nd line SNRI (duloxetine or venlafaxine). If both contraindicated or intolerable then Pregabalin.

Review effectiveness and ADR every 2-4 weeks during first 3 months then every 3 months.

Counsel on common effects during treatment initiation (suicidal thoughts and worsening of anxiety) but importance of reporting this instead of withdrawing from drug

SSRI – don’t take NSAIDS or if prescribed take with PPI

For pregnant women step 3

DO NOT give benzo or antipsychotics in primary care

Benzodiazepines (SCH 3 and 4)

Most commonly used anxiolytics and hypnotics

Short rem relief (2-4 weeks only) of anxiety that is severe, disabling, or causing the patient unacceptable distress

use to treat short-term ‘mild’ anxiety is inappropriate

Sch 4 CDs, apart from temazepam

Sch 3 (CD no register) and midazolam

Pharmacological effects of benzodiazepines

Sedation, sleep induction

sleep, but can still cause arousal

decreased anxiety, amnesia at higher doses

muscle relaxation (both midbrain and spinal effects)

anticonvulsant activity

Reduced aggression

Depression

Persistent low mood and/or loss of pleasure in most activities and range of emotional, cognitive, physical, and behavioural symptoms

Diagnosis

Low mood

Loss of interest/pleasure from normally pleasurable activities (anhedonia)

Reduced energy (fatigue)

Low self-esteem; feelings of guilt

Inability to think/concentrate

Altered psychomotor activity

Sleep disturbance; early morning wakening

Altered appetite

Suicidal thoughts

Diagnosis requires 2 core symptoms plus 2 or more others present for most of the day on most days for the last 2 weeks

Differential diagnosis

Ensure symptoms are not caused by physical illness, alcohol, medication, or illicit drug use

The symptoms aren’t caused by normal grief (death of family) – maybe consider very long grief

Never been a manic (severe levels of high mood) or hypomanic (to a reduced level) episode

Treatment

Dependant on accurate assessment and diagnosis of depression

Psychological

CBT, behavioural activation, interpersonal psychotherapy, problem solving therapy

Social

Identify stressors and work on strategies/signposting to other supporting organisations

Biological – moderate to severe

Antidepressant therapy or antidepressant and antipsychotic combination therapy in psychotic depression

Drug classes

Tricyclic antidepressants (TCAs) e.g., amitriptyline

Selective serotonin reuptake inhibitors (SSRIs) e.g., fluoxetine

Serotonin and NA uptake inhibitors (SNRIs) e.g., venlafaxine

Monoamine oxidase inhibitors (MAOIs)

Irreversible e.g., phenelzine (MAO-A and B)

Reversible e.g., Moclobemide

Atypical antidepressants e.g., Mirtazapine

Noradrenaline reuptake inhibitors (NRIs) e.g., Atomoxetine

TCA - S/E – Short lasting (days) sedation, confusion, and Incoordination in both normal and depressed patients, antimuscarinic effects, dry mouth, blurred vision, decreased mucus production. Dangerous CV effects in OD 

Severe depressive at risk of suicide shouldn’t be given TCA

Interactions – potentiation of the effects of alcohol – alcohol is a depressant and will only compound the depressive effects

SSRI’s - S/E – nausea, anorexia, insomnia, and loss of sexual function

Less anticholinergic side-effects and less dangerous in OD than TCAs. Prolonged QTc – cardiovascular complications risk with citalopram  interactions – NSAIDs, Anticoagulants, triptans

SNRI’s - S/E – significant withdrawal effects – have short half-lives so need to be taken regularly to avoid these effects. Complex nature of TCAs makes them difficult to prescribe to complex patients unlike SNRIs

Interactions – NSAIDs and anticoagulants

MAOIs - S/E – antimuscarinic effects, restlessness as a result of CNS excitation

Interactions – serious food and drug reactions e.g., cheese (tyramine from food such as cheese is broken down by MAO. The lack of breakdown from MAOIs can lead to tyramine actively displacing neurotransmitters such as 5HT, DA, NA – causing hypertensive crisis

VERY IMPORTANT COUNSELLING POINTS

No other drugs or illicit drugs with this

Side effects

Drug and food interactions are unacceptable.

“Cheese reaction”: this occurs when amines that are generated during fermentation, like tyramine, are ingested and absorbed from the gut. (The main danger is ripe cheese, yeast products - Marmite).

Large rise in systemic tyramine indirectly results in a large release

    of catecholamines

Hypertensive crisis characterised by throbbing

            headache, tachycardia & cardiac arrhythmias.

Same can occur with drugs (Pseudoephedrine)

Atypical antidepressants - S/E- sedation, weight gain, increased appetite – good in patients with anorexia or depression causing loss of appetite or weight

Blood disorders – counselling

Withdrawal issues

Can be used with other antidepressants that cause sleep issues

Interactions – alcohol

FDA black box warning – suicide

Treatment

Mild symptoms – psychological therapy

Persistent mild symptoms or moderate to severe symptoms – combination of psychological and drug therapy

1st line treatment usually SSRIs

2nd line switch to alternate SSRI

3rd line switch to different class (normally an SNRI)

Practical issues

Initiating an antidepressant can cause feelings of anxiety consider co-prescribing short course of benzodiazepines to counteract the anxiety

During the first few weeks of antidepressant treatment can have worsening suicidal thoughts with improved motivation so ensure counselling and regular reviews

Consider prescribing limited supply of meds to reduce chance of OD

Side effects often transient and improve with time

Caution when switching antidepressants – table of different half-lives and how to taper them

Treatment approach

If no response to 3 antidepressants, then check concordance, review diagnosis, and consider if social problems are maintaining depression

Consider augmentation – addition of drug to the current therapy

Mirtazapine – sleep

Quetiapine – mood

Aripiprazole

Lithium – mood stabiliser

Lamotrigine – mood stabiliser

Electroconvulsive therapy

Response

2-4 weeks usually for response to be seen (longer in elderly)

Improvement greatest during weeks 1-2

If no response during 2–4-week period, consider first increase in dosage then if again limited efficacy, then switch to alternative

Extended duration if treatment trial will lead to additional benefit in some

Differences between drugs

Mirtazapine, escitalopram, venlafaxine, and sertraline

more efficacious than

duloxetine, fluoxetine, fluvoxamine, paroxetine and reboxetine

Reboxetine less effective overall

Escitalopram and sertraline

better tolerated than

duloxetine, venlafaxine, fluvoxamine, paroxetine and reboxetine

Preventing relapse

Relapse rate 3-6 months post remission is 50% with no drug treatment

A/D treatment reduces absolute risk of relapse by about 50%

After 1st episode continue for 6-9 months

After 2nd episode continue for 12 months

After 3rd episode continue for 2 years

Insomnia – difficulty in getting to sleep or staying asleep long enough to feel refreshed the next morning

Causes

Recreational drugs

caffeine, nicotine, alcohol, cannabis)

Medicinal drugs

anticonvulsants, antipsychotics, b-blockers, SSRIs, MAOIs, steroids, decongestants, Alpha agonists and antagonists, narcotic analgesics

Drug withdrawal

from CNS depressants (eg alcohol, anxiolytics/hypnotics)

Physiological

Diet, late night exercise, shift work (night and evening work)

Environmental

Noise, bright lights, extremes of temperature

Medical conditions

Psychological - anxiety, depression, grief, stress

Non-psychological eg chronic pain, gastric reflux, asthma, sleep apnoea

Types of insomnia

Primary insomnia - insomnia not attributable to a medical psychiatric or environmental cause

Secondary insomnia- insomnia secondary to another condition

Transient (2-3 days) – caused by changes in routine (for eg. change in time zone, alteration of shift work)

Short term (<3 weeks) – may result from temporary environmental stress

Chronic insomnia (>3 weeks) –usually secondary to other conditions

Treatment

FIRST LINE IS ALWAYS NON-DRUG treatments e.g., lifestyle changes and CBT

Drug therapy – Hypnotics

Benzodiazepines

Benzodiazepine-like drugs (Z-class)

melatonin

BEFORE hypnotic is prescribed the cause of insomnia must be established and where possible, underlying factors should be treated

NICE recommends

if hypnotic medicine is the appropriate way to treat one for only short periods of time and strictly according to the licence for the drug. (Usually, 1-2 weeks and max 4 weeks) and should be prescribed on a weekly basis

Benzodiazepines

 Most benzodiazepines

decrease time taken to get to sleep

in individuals who habitually sleep <6hr, the drug increases duration of sleep

Few short-acting BDZs recommended for insomnia (short-term treatment – max 2-4 weeks)

Should only be used when SEVERE, DISABLING or causing EXTREME DISTRESS

Benzodiazepine – like drugs

Z -Hypnotics – Zaleplon, zopiclone, zolpidem (Short acting – t1/2 < 8 hr)

Short term use only (2-4 weeks)

Lack of anxiolytic effects –drowsiness or dizziness - just induce sleep

Melatonin treatment

Prolonged release melatonin available for primary insomnia in over 55yr olds (can be used up to 3 weeks)

Antihistamine gen 1 – can cause drowsiness

Anxiolytics

Kalms, Kalms day, Karma, Karmamood, Potters Newrelax, Relaxherb, Stressless

Hops, valerian, passionflower, passiflora, vervain, St John’s Wort

Sedatives

Kalms night, Kalms sleep, Dormesean, Niteherb, Nytol herbal, Potters Nodoff, sominex herbal

Hops, valerian, vervain, skullcap, wild lettuce, passiflora

Some herbal remedies do contain active ingredients so be careful of interactions

Lifestyle changes – promote sleep hygiene

establishing fixed times for going to bed and waking up

trying to relax before going to bed

maintaining a comfortable sleeping environment avoiding napping during the day

avoiding caffeine, nicotine, and alcohol late at night 

avoiding exercise within four hours of bedtime 

avoiding eating a heavy meal late at night

avoiding watching or checking the clock throughout the night

using the bedroom mainly for sleep if possible

avoid going on phone, looking at screens immediately before bed or whilst in bed

ADHD

Persistent developmentally with inappropriate levels of over reactivity, inattention and/or impulsivity

Diagnosis – based on observation there are no biomed tests

Symptoms – 9 symptoms across 2 domains

Hyperactivity/impulsivity

Inattention

Can be combined type or dominant in one

ADHD – Predominantly inattentive type

Fails to give close attention to details or makes careless mistakes.

Has difficulty sustaining attention.

Does not appear to listen.

ADHD – predominantly Hyperactive/impulsive type

Fidgets with hands or feet or squirms in chair.

Acts as if driven by a motor.

Blurts out answers before questions have been completed.

Difficulty waiting or taking turns.

Interrupts or intrudes upon others.

ADHD – Combined type

Patient meets both sets of inattention and hyperactive/impulsive criteria

ADHD – Differential diagnosis

Sensory impairment – leading to under or over-sensitivity to triggers

Epilepsy and related states – could present as inattention

Effects of head injury

Acute or chronic medical illness

Poor nutrition – linked to poor behavior – not directly linked to ADHD

Sleep disorders – linked to poor behavior – not directly linked to ADHD

Side effects of medication

School or classroom difficulties – bullying or other factors

Large links to exposure to smoking and drinking during pregnancy, childhood illness such as meningitis or other viral infection, low birthweight/prematurity. HIGH heritability

Treatment

Mild-moderate –1st line - parent-training/education programmes with parent and child, group based or individual sessions. Teachers receive ADHD training and offer intervention in schools.

2nd line – CBT or social skills training

3rd line – DRUG THERAPY ONLY FOR SEVERE and should be offered along with psychological, behavioural, and educational interventions

Drug therapy

Methylphenidate – generally first choice

Atomoxetine - if other tics, Tourette's syndrome, anxiety disorder, stimulant misuse or risk of stimulant diversion are present

D-amphetamine – ONLY if other drugs ineffective at raised doses – CD2 high risk in addiction and dependence and misuse so used as last resort

Decide which drug treatment to use based on:

their different adverse effects

potential problems with compliance (for example, if a mid-day dose is needed at school)

potential for drug diversion (taken by others) and misuse

preferences of the child or young person and their parent or carer

When a decision has been made to treat children or young people with ADHD with drugs, healthcare professionals should consider: –

methylphenidate for ADHD without significant comorbidity

methylphenidate for ADHD with comorbid conduct disorder

methylphenidate or atomoxetine when tics, Tourette’s syndrome, anxiety disorder, stimulant misuse or risk of stimulant diversion are present

atomoxetine if methylphenidate has been tried and has been ineffective at the max dose, or the child intolerant to low or moderate doses of methylphenidate.

Atomoxetine

Closely observe children or young people taking atomoxetine for agitation, irritability, suicidal thinking, and self-harming behavior, particularly during the initial months of treatment, or after a dose change.

Liver damage in rare cases (usually presenting as abdominal pain, unexplained nausea, malaise, darkening of the urine or jaundice).

Treatment of adults

In adults, methylphenidate normally first line treatment

Consider atomoxetine or dexamphetamine if symptoms do not respond to methylphenidate or the person is intolerant to it ~6 weeks.

Selection of appropriate medication

Immediate-release preparations if more flexible dosing is required or during initial titration to using methylphenidate, consider determine correct dosing levels

If there is a choice of more than one drug, use the drug of lowest overall cost

modified-release preparations for convenience…

their pharmacokinetic profile,

improving adherence,

reducing stigma (because the drug does not need to be taken at school)

reducing problems of storing and administering controlled drugs in schools

abuse liability

AUTISM

Symptoms

Socialization

Impaired use of non-verbal behaviors to regulate interactions

Delayed peer interactions, few or no friendships, and little interaction

Absence of seeking to share enjoyment and interests

Delayed initiation of interactions

Little or no social reciprocity and absence of social judgment

 Communication

Delay in verbal language without non-verbal compensation (gestures)

Impairment in expressive language and conversation, and disturbance in pragmatic language use

Treatments

NEED early diagnosis and defined biomarkers

Currently intervention is through family and educational support

Only some specific programs have an evidence base

Aim is to ‘improve the functional status…through skill acquisition in core areas’

Eg developing relationships

Achieving social and environmental milestones through play

Positive reinforcement of social communication

Pharmacological treatments for co-morbidities

Developmental

Hyperactivity/impulsivity (see ADHD)

Psychiatric

SSRIs, other antidepressants for depression

atypical antipsychotics for OCD

SSRI or a2 agonists for anxiety

Behavioural

Atypical antipsychotics (irritability, aggression)

Sensory

Neurological

anticonvulsants and fits, a2 agonists for tics

Gastrointestinal

Sleep disruption

melatonin and clonidine

Dementia

Symptoms –

Higher cognitive function affected

Memory, thinking, comprehension, learning capacity, language (speaking and understanding it)

Daily living activities/emotional behaviour (non-cognitive symptoms)

Behavioural and psychological symptoms of dementia (BPSD) – include agitation, apathy, depression, anxiety, delusions, hallucinations, irritability, and wandering

Treatment -

Acetylcholinesterase (AChE) inhibitors (donepezil, galantamine, and rivastigmine) — as monotherapies for managing mild to moderate Alzheimer's disease.

Memantine (a N-methyl-D-aspartic acid receptor antagonist):

As monotherapy for managing Alzheimer's disease for people with moderate Alzheimer's disease who are intolerant of, or have a contraindication to, AChE inhibitors, or for people with severe Alzheimer's disease.

In addition to an AChE for people with established moderate or severe Alzheimer's disease who are already taking an AChE

For people with non-Alzheimer's dementia the use of AChE inhibitors or memantine is unlicensed, but they may be prescribed by a specialist for people with:

Mild to moderate dementia with Lewy bodies:

Donepezil or rivastigmine are recommended first line.

Galantamine is an option if donepezil and rivastigmine are not tolerated.

Severe dementia with Lewy bodies:

Donepezil or rivastigmine are recommended.

Vascular dementia:

AChE inhibitors or memantine are options if the person has suspected comorbid Alzheimer's disease, Parkinson's disease dementia, or dementia with Lewy bodies.

Risperidone and haloperidol are the only antipsychotics licensed for treating non-cognitive symptoms of dementia, although other antipsychotics are often prescribed off-label for this purpose.

Acetylcholinesterase inhibitors

NMDA receptor antagonist

Cholinesterase inhibitors for mild to moderate AD (eventually stop working)

NMDA receptor antagonist for severe AD and moderate AD in some cases

Treatment must be started only by a specialist clinician

Rheumatoid arthritis

Inflammatory disease causing persistent symmetric joint synovitis

Presents as pain and joint stiffness with heat and swelling progressing at rest and after periods of inactivity with malaise, fatigue, fever, and weight loss

Risk factors – smoking, eating large amounts of red meat, drinks excessive coffee

Symptoms

Joints

Pain

Swelling

Stiffness

Systemic

Fatigue, depression, irritability

Anaemia

Flu-like symptoms, such as feeling generally ill, hot, and sweating

Pain worse in morning

Treatment

Drugs, mild exercise (enhance flexibility of joint and muscle strength), lifestyle changes (rich antioxidant diet, no smoking)

Main types of RA meds

NSAIDs (short term symptomatic relief) – reduce inflammation. OTC (ibuprofen, naproxen). POM (celecoxib, etoricoxib)

S/E – GI irritation, ulcers (use at lowest dose and take with food, use PPI to lessen effects)

Caution – asthmatics and renal impairment and patients with increased CV risk

Disease-modifying anti-rheumatic drugs (DMARDs) – 1ST LINE for active RA (methotrexate, sulfasalazine)

S/E – Nausea, diarrhoea, oral ulceration, alopecia, cough, SOB, bone marrow suppression – CAN BE REDUCED by co-prescribing FOLIC acid 1mg daily

Biological therapies (type of DMARD) – used when DMARDS don’t control RA

Glucocorticoids – short term treatment when starting new DMARD for rapid symprom control  - also used in flares

Analgesics (painkillers)

Drug Treatment Schedule

Start two DMARD regime once diagnosed, using titration regimens

Use anti-inflammatories (NSAIDs), paracetamol with or without corticosteroids until effective

Review after 6 months: increase dose or switch as clinical condition determines.

Patient counselling in RA

Place of drugs in therapy

Onset of action

Side effects

Immunosuppression

Regular painkillers

Regular monitoring including blood tests

Dexterity aids, prescription services

Osteoarthritis

Predominantly non-inflammatory and caused by cartilage loss from synovial joints and bone remodelling due to excessive and repeated overloading on weight bearing joints or stress of a joint over tome and specific injuries

Risk factors – genetic, age, gender, obesity, damage, occupational, and stress

Symptoms

Pain – tends to be worse when using the joint and at end of the day (Worsens on use, resolves at rest)

Stiffness – feel stiff after rest, usually wears off as you get moving

Grating or grinding sensation (crepitus) – joints creak or crunch as you move

Swelling – may be caused by osteophytes (bone outgrowth) or caused by synovial thickening and extra fluid

Muscles around joint look thin/wasted

Unable to use joint normally – doesn’t move as freely or far as normal

Joints give way – muscles have weakened, and joint is less stable

Management

Provide information on sources of advice and support

Advice on self-care strategies such as;

Weight loss, local muscle strengthening exercises and aerobic fitness training

Appropriate footwear, local heat, or cold packs

Odder psychosocial support – career and occupational health assessments if needed

Advice on simple analgesia

Arranging regular reviews to assess response to treatment

MANAGEMENT GOAL – pain reduction and symptomatic relief

First line:

Paracetamol regularly – 4g daily

Topical NSAIDs

Additional treatment:

Oral NSAIDs– not first line

-Start with ibuprofen

-Monitor for side effects

-Possible place for topical therapy

Topical capsaicin – adjunct and helpful in knee and hand – works by stimulating then decreasing the pain sensation

Corticosteroid injection: â pain and inflammation of flare-up

Role of pharmacist

Counselling:

dosage regimen

side effects

warnings

Monitoring for side effects

Weight loss advice

Physiotherapy advice

Compliance aids & living aids

Gout

Type of inflammatory arthritis – causes severe pain and damage to joints

Caused by abnormal high levels of uric acid in blood which deposits urate crystals in joints and tissue

3 phases

Asymptomatic hyperuricaemia – can remain in this stage for life

Acute attack of gouty arthritis – can vary from months to years before another attack

Final period of chronic tophaceous gout – nodules effecting joints

Treatment

Acute

Ice

Rest affected joint

NSAIDs – short term, 7-14 days, high dose, for pain relief and anti-inflammatory

Colchicine (Dose: 500mcg 2-4 x daily until symptomatic relief or SE (stomach cramps, diarrhoea, vomiting)), steroids (used when NSAID and colchine is contraindicated or not useful)

Choice of drug dependant on comorbidities and renal function (NSAID cause fluid retention whereas colchicine doesn’t)

Colchicine use limited as it can have sudden toxicity at higher conc

Combination treatment can be used as well if monotherapy isn’t controlling the attack

Long term treatment to reduce urate

Lifestyle modifications (reduce dietary intake)

Drug therapy: Allopurinol (1st line – offer to all, 100mg od, increased in 100mg increments every 2-3 weeks) S/E – rashes

Febuxostat (2nd line only use when allopurinol intolerant or contraindicated – 60mg OD dose)

Monitor urate level – aim for < 360 μmol/L or 6 mg/dl (critical level)

Muscoskeletal

Sprain

Commonly ankle, wrist, thumb, knees – pain, swelling, tenderness, bruising, disabled use and no weight

Strain

Common in legs and lower back – pain, swelling, bruising, red, and reduced function

BOTH

Self-limiting gets better in 4-6 weeks and full recovery in 12 weeks

Non-pharma advice

PRICE (Protect, Rest (48-72hrs), Ice immediately after, Compression bandages and Elevate to reduce swelling

Reduce HARM (Heat, alcohol, running and massaging for 72hrs.

Avoid NSAIDs for 72hrs

Exercises for sprains

Gently move joint in all directions to increase and maintain flexibility (lack of movement can delay recovery BUT severe sprains with complete lack of movement rest for 10 days first)

Treatment – topical and oral analgesics

Refer – severe pain, possible break or fracture, no alleviation with OTC meds

Lower back pain

Symptoms – pain, tension, soreness, stiffness without underlying cause

6 weeks usual recovery can be up to 12 weeks

Advice

Back exercises, improve posture, yoga, avoid lying or sitting for too long, remain active.

Sleep in different positions, pillows between legs, under knees, hot baths, hot water bottles, ice packs.

Treatment

OTC – topical analgesics or co-codamol if still painful

Refer

No improvement in 3 days, continues for more than 6 weeks, pain travels higher, pain after injury, younger than 20, older than 50, pain affects sleep, unsteady on feet, unexplained weight loss

EMERGENCY

Pins and needles in back, genital, bum, both legs, lose urine or bowel control

Conjunctivitis

Symptoms

Bacterial

Viral

Allergic

Eyes affected

1 or 2

Both

Both

Discharge

Pussy

Watery

watery

Sensation

Gritty

Gritty

Itchy

Co-presenting symptoms

None

Cough/cold

Rhinitis

If pussy, red or gritty it is contagious – allergic ISNT contagious

Advice

Don’t wear contacts, hold cold flannel on eyes for few mins to cool them, use FBC water to gently wipe lashes and clean off crust and clean with cotton wool pad. Use a different one for each eye

Control spread by – reg wash hands with hot soapy water, cover mouth and nose when sneezing, don’t share towels or pillows and don’t rub eyes

Refer

Baby less than 28 days old with red eyes, allergic reaction, or spots on eyelids. For all – symptoms not resolved after 2 weeks

111 - Severe pain, sensitive to light, sudden changes to vision

Treatment

Viral – self-limiting, use hygiene and non-pharma advice

Allergic – Opticrom eye drops (Adults and child – 1-2 drops in each eye up to 4x daily)

Bacterial – over 2, chloramphenicol drops/ointment (Optrex Bacterial Conjunctivitis 1%w/w Eye Ointment) - apply a small amount of ointment in the affected eye 3-4 times daily for 5 days

Blepharitis

Symptoms

NOT contagious, rims of eyelids are inflamed, burning, soreness or stinging in the eyes, crusty lashes that stick together, itchy eyelids

Advice

Clean eyelids at least 1x daily, clean eyes even if symptoms clear, don’t wear contacts, or eye makeup

Cleaning eyes – soak a clean flannel/cotton wool in warm water and place on eye for 10 mins, gently massage eyelids for 30 secs, clean lids using cotton wool. Baby shampoo at 10:1 ratio good.

Refer

No improvement after 2 weeks of cleaning eyes

Treatment OTC

Brolene eye drops – 1-2 drops in each eye up to 4 x daily. If not better in 2 days refer

Dry eyes

Symptoms

Dry feeling, sensation of something in eye, burning, grittiness, itching, light sensitivity, over-blinking, redness, excess tears (randomly tearing)

Causes – over 50, contacts, digital screens, AC, windy/cold/dry/ dusty environment, smoking, alcohol, meds (antidepressants/BP) medical conditions (blepharitis)

Refer

Treatment failure after 2 weeks, change in eyelid shape

111 – severe pain and red, contact wearer with red eyes (could be an infection)

999 A&E – sudden change in sight, bursts of light sensitivity, severe headache/nausea, dark red eyes, injured/pierced eye, something stuck in eye

Advice

Clean eyes daily, take breaks when using screens, use screens below eye level, use humidifier, wear glasses instead of contacts

Treatment 

Light lubricant – Optrex Double Action Drops for Dry and Tired Eyes - Apply 1-2 drops in each eye.

Hyaluronic Acid - Artelac Rebalance Drops, long lasting relief - Place 1 drop into the conjunctival sac 3-5 times daily or more frequently if required.

Hypromellose drops – 1-2 drops 3 x daily

Excessive ear wax

Symptoms – hearing loss, earache, noise/ringing, vertigo, dizziness, and nausea

Causes – narrow/damaged canals, hairy canal, skin condition affecting scalp around ear, inflammation of ear canal

Refer – not cleared in 5 days, badly blocked, severe, complete loss of hearing, likely infection

Advice – don’t use fingers or cotton buds to remove wax

Treatment

Olive oil drops – 2-3 drops in affected ear and massage around outside of ear BD x 7 days

Use dropper when lying down with head to one side to allow oil into ear, over 2 weeks then lumps should fall out, but symptoms should be better within 5 days

Otitis externa

Symptoms - pain, discharge, itch, irritation, external ear/canal appears red, swollen, eczema, deafness, skin swells, tender to touch

Refer – ear pain in children, inflamed pinna, unsuccessful treatment (after 4 days), hearing aids, excessive discharge (wax or pus), high fever, vomiting, fatigue, confusion, dizzy, stiff neck, rash, slurred speech, fits, light sensitivity

Advice – avoid under/over dressing feverish child, lower heating, offer regular fluids, avoid dummies when lying flat, give paracetamol/ibuprofen if child is unwell/distressed (not together)

Treatment

Acute localised (furunculosis) – infected hair follicles in outer-ear causing swelling and irritation

Treatment – hot flannel, oral analgesics, antibiotics if severe

Acute diffuse (over 3 months – more widespread inflammation of skin, bacterial/fungal infection or contact dermatitis due to irritant/allergens

Treatment – earwax plus or EarCalm

Otitis media

Symptoms – earache, discharge, hot, irritable, sleeplessness, ear pulling/rubbing, crying, temporary deafness

Refer – recurrent infections, no improvement in 3 days

Treatment

Self-limiting should be better in 3 days, single analgesics for pain

Hyperthyroidism

Too much thyroid hormones produced naturally

Symptoms

Tremor, warm sweaty palms, weigh loss despite increasing appetite, heat intolerance, diffused alopecia, hair thinning, tachycardia, diarrhoea

Advice

Healthy diet with foods rich in antioxidants, green leafy vegetables (broccoli, cabbage etc)

Vitamin D, omega 3 fatty acids and calcium rich foods. Smoking cessation

Treatment

Carbimazole (adjunct B blocker propylthiouracil for adrenergic symptoms) – block and replace regime

Combo of fixed high dose carbimazole and levothyroxine

Radioactive iodine destroys thyroid cells, surgery to remove some thyroid

Hypothyroidism

Thyroid gland doesn’t produce enough hormones caused by immune system attacking thyroid gland and damaging ait or by damage to thyroid that occurs during treatments for a hyperthyroidism or thyroid cancer

Symptoms

Fatigue, muscle pain, weakness, weight gain, sensitive to cold, dry skin, brittle hair, nails, depression, reduced libido

Advice

Eat antioxidant rich food, seeds and nuts, tyrosine (meat, dairy, legumes)

Avoid – soy, iodine rick food, leafy green vegs, caffeine, alcohol – quit smoking, alcohol.

Inform GP if pregnant (needs treatment and monitoring during)

Treatment

Levothyroxine 1st line – dose depends on blood test and progression – take tablet at same time every day (MORNING) If taking too much causes sweating, chest pain, headaches, diarrhoea, vomiting. Supressing thyroid supressing hormone with high doses causes atrial fibrillation, stroke, osteoporosis

Cold sores

Symptoms

Simplex - Pain, burning, itching, tingling before lesions and lasts 6-48 hrs

Crops of vesicles burst and crust over and heal, commonly on lower lip and ends of mouth

Gingivostomatitis – fever, malaise, sore throat, painful nodules in cervix or under jaw, excessive salivation. Painful vesicles on a red swollen base that rupture to form ulcers inside mouth, covered with yellow/grey membranes

Refer – immunocompromised, unable to swallow, risk of dehydration, severe infection, complication, pregnant, recurrent

Treatment

Paracetamol/ ibuprofen for symptoms

Topical acyclovir/penciclovir OTC – use from onset of symptoms before lesions until lesions heal

OTC topical anaesthetic or analgesics, mouthwashes, or lip barriers – topical analgesics aren’t licensed in children

DON’T prescribe oral antiviral for healthy people

Consider prescribing oral antiviral for healthy people with episode of primary oral herpes simplex, recurrent labialis if lesions are severe, frequent, or persistent and recurrent

And for those who are immunocompromised

Should take at onset and until lesions have healed – minimum of 5 days

Choice of aciclovir or valaciclovir based on preference, dose, regimen, and adherence

Advice

Reassure its usually self-limiting and heals without scarring

Adequate fluid intake

Offer leaflets or websites for more info

Avoid kissing, oral until lesions fully healed, don’t share pillows, makeup, or lip balms. Don’t touch lesions other than when applying treatment – dab instead of rubbing. Wash hands after touching.

Athletes foot

Interdigital — most common; affects the lateral toe web spaces first; usually caused by Trichophyton rubrum.

Moccasin or dry — diffuse chronic scaling and hyperkeratosis affecting the sole and lateral foot; usually caused by Trichophyton rubrum.

Vesicobullous — least common; multiple small vesicles and blisters mainly on the arches and soles of the feet; usually caused by Trichophyton interdigital.

Risk – hot, humid, occlusive footwear excessive sweating, contaminated surfaces, immunocompromised

Advice

Wear well fitting, open footwear that keep feet cool and dry, replace old shoes that may be contaminated. Maintain good foot hygiene – wear different pair of shoes every 2-3 days. Wear cotton, absorbent socks, don’t scratch skin, after washing feet dry then well and between toes, don’t share towels and wash towel freq.

Treatment

Topical antifungal cream in mild, non-extensive disease

Terbinafine 1% cream (12 and over – apply thinly to affected area 1 or 2 daily for 7 days) or clotrimazole 1% cream (2-3 times daily and continue for 4 weeks minimum) okay for kids – OTC for some ages

Additional mild topical corticosteroid if there’s inflammation

Hydrocortisone 1% cream (OD for max 7 days)

Adult severe or extensive – oral antifungal with confirmed fungal infection

1st choice – terbinafine (250 mg once daily for 2–6 weeks, depending on the severity of infection)

2nd – itraconazole, Griseofulvin if not tolerated or contraindicated

Refer

Treatment failure, severe pain, got, painful and red (indicative of serious infection), infection spreads, diabetic patient, immunocompromised

Warts and verrucae

Warts – small, rough growths caused by infection of skin with HPV, form anywhere on skin most commonly on hand and feet

Verruca – (plantar wart) wart on sold of feet

Spread by direct contact, occur and clear spontaneously at any time or may take years

Common warts are firm and raised with a rough surface that resembles a cauliflower (common on knuckles, knees, and fingers).

Periungual warts are common warts around the nails that can be painful and disturb nail growth — nail biting is a risk factor.

Plane warts are usually round, flat-topped, and skin coloured or greyish yellow (common on the backs of hands).

Filiform warts have a finger-like appearance and may have a stalk (more common on the face and neck).

Palmar and plantar warts grow on the palms and the soles of the feet (verrucae). They often have central dark dots (thrombosed capillaries) and may be painful.

Mosaic warts occur when palmar or plantar warts coalesce into larger plaques on the hands and feet.

Not harmful and don’t come with symptoms and resolve with treatment

Advice

Reducing transmission and limit spread, keep feet dry, wear slippers or waterproof plaster in shower and communal areas. don’t share towels, socks, shoes. Don’t scratch lesions, bite nails or suck fingers with warts

Refer

Painful, facial, uncertain diagnosis, immunocompromised, extensively infected

Treatment

Only treated if painful, cosmetically unsightly, or patient request and persistent as the treatment is long and can have side effects.

Topical salicylic acid – up to 12 weeks

Duofilm® (salicylic acid 16.7% plus lactic acid 16.7%) — licensed for plantar and mosaic warts.

Bazuka® extra strength gel (salicylic acid 26%) — licensed for warts and verrucae.

Occlusal® (salicylic acid 26%) — licensed for common and plantar warts.

Salactol® (salicylic acid 16.7% plus lactic acid 16.7%) — licensed for warts, plantar warts, and verrucae.

Apply OD at night, file and soften area by soaking in warm water for 5-10 mins, peel of remaining film before administering next dose, don’t apply on healthy skin

Cryotherapy – every 2 weeks for max 6 treatments

Liquid nitrogen – only for older children and adults

Corns and calluses

Hard or thick areas of skin that can be painful

Corns – lumps of hard skin on knuckles and joints of toes

Callouses – larger patches of rough, thick skin

Both can be tender and painful

Refer

Diabetic, heart disease, circulation issues. Bleeding or puss, treatment failure after 3 weeks, severe pain

Advice

Wear thick, cushioned socks, wear wide, comfortable shoes with low heel and soft sole, use insoles or heel pads, soak corns and calluses in warm water to soften them, use pumice stone regularly or foot file to remove hard skin. Moisturise.

Don’t try to cut them, walk, or stand for long period, wear high heels or tight pointy shoes, go barefoot

Treatment

Heel pads and insoles, OTC products, pain relief

Carnation brand caps for both – adhesive dressing

Fungal nail infection

Caused by dermatophyte and non-dermatophyte moulds and yeasts

Symptoms

Discoloured, abnormal, small flaky white patches and pits on top of nail and becomes rough and eroded. Nail lifted, wite or yellow opaque streaks on one side of nail, scaling, thickening

Refer

Diabetic, severe, treatment failure, spread to other nails

Advice

Keep nails trimmed short and filed, don’t share clippers and files. Well-fitting shoes, cotton socks, maintain good foot hygiene, weak shoes in communal places, avoid nail trauma

Treatment

Not needed if patient not troubled by appearance and infection is asymptomatic

Advise antifungal treatment if – walking uncomfortable, distress, cosmetic, co-morbid complication, or complication

If dermatophyte or candida infection conformed – topical antifungal treatment 0f 50% of nail involved, 2 nails infected, contraindication to oral antifungal

Topical – amorolfine 5% mail lacquer – OTC apply 1 or 2 weekly to affected nail after gentle nail filing – 6 months minimum for fingernails, 12 months for toenails

If dermatophyte nail infection is confirmed:

Prescribe oral terbinafine first-line.

250 mg once a day for between 6 weeks and 3 months for fingernails, and for 3–6 months for toenails

Oral itraconazole if an alternative drug is indicated.

Prescribe as pulsed therapy 200 mg twice a day for 1 week, with subsequent courses repeated after a further 21 days.

If Candida or non-dermatophyte nail infection is confirmed:

Prescribe oral itraconazole first-line.

Prescribe as pulsed therapy 200 mg twice a day for 1 week, with subsequent courses repeated after a further 21 days.

Prescribe oral terbinafine if an alternative drug is indicated.

Prescribe 250 mg once a day for between 6 weeks and 3 months for fingernails, and for 3–6 months for toenails.

[pacehpstuff]

HbA1C Test - Indications, Range & Cost

HbA1c test, also known as glycated haemoglobin A1c, is used to measure the blood sugar levels in the body, which aids in diagnosing and managing diabetes mellitus. The HbA1c blood test value (denoted in percentage) indicates the average blood sugar level for the past 2–3 months. The HbA1c test normal range includes values between 4 and 5.7%; less than 6.5% indicates prediabetes, and an HbA1c value of 6.5% or more indicates hyperglycaemia (diabetes mellitus).

HbA1c test uses

In general, healthy persons contain glycated haemoglobin; however, in prediabetics or diabetics, the excess amount of unutilised sugar molecules present in the blood (which might occur due to insulin resistance or absence of insulin production) attaches to the haemoglobin, resulting in higher levels of glycosylated haemoglobin. The amount of glycohemoglobin produced is directly proportional to the mean blood glucose during the 8-10-week period prior to the initiation of the HbA1c test, which thereby provides an average of 2-3 months days of blood sugar levels.

The blood sugar test HbA1c is used to screen and diagnose the following conditions:

Diabetes mellitus

Prediabetes

Accurate HbA1c testing is crucial when it comes to managing your diabetes or blood sugar levels. At PACE Hospitals in Hyderabad, you can be confident in receiving the best care for this vital test. Our state-of-the-art NABH accredited labs utilize cutting-edge technology to deliver precise results. Our experienced best endocrinologists, diabetologists and dedicated healthcare team interpret your HbA1c levels and guide you towards personalized treatment plans, empowering you to manage your diabetes effectively.

Importance of HbA1c test

The Hemoglobin A1c (HbA1c) test is a crucial tool in managing diabetes. It provides a measure of a person's average blood sugar levels over the past two to three months, offering valuable insights into long-term glucose control. This test is essential for monitoring and adjusting treatment plans, reducing the risk of diabetes-related complications, and promoting overall health in individuals with diabetes.

HbA1c test indication

For screening, diagnosis or managing diabetes, one might opt for an HbA1c test in the following scenarios.

Screening:

Patients over the age of 45

Overweight patients under the age of 45 and having one or more risk factors for prediabetes or type 2 diabetes.

Second test: If the patient is asymptomatic but still has an HbA1c value between 5.7% and 6.4% (prediabetes) or more than that (diabetes), a second test is recommended on a different day.

HbA1c test: Once every 1 to 2 years: In patients who are prediabetic and taking measures to control and lower the risk of diabetes mellitus.

HbA1c test: Once every 3 years: In normal HbA1c patients with age over 45 and having associated risk factors or ever had a history of gestational diabetes

In managing diabetes: In patients with uncontrolled diabetes and are on oral antidiabetic medications, the best time for HbA1c test, as per the American Diabetes Association (ADA) suggestions, is once every three months. In the case of stable and well-controlled patients, the sugar test HbA1c should be performed once in every six months.

Accurate HbA1c testing is crucial when it comes to managing your diabetes or blood sugar levels. At PACE Hospitals in Hyderabad, you can be confident in receiving the best care for this vital test.

PACE Hospitals is one of the best hospital for HbA1c test in Hyderabad, Telangana, India for quality, accuracy, and personalized care. Let us help you stay on track towards a healthier you. Choose PACE Hospitals for a comprehensive diabetes care experience, from accurate diagnosis to expert guidance, all under one roof.

[myacare]

Worldwide Statistics from the American Diabetes Association state that a person loses a limb due to diabetes-related complications every 30 seconds. According to a 2019 Statista report, Germany had the highest prevalence of diabetes in Europe among their adult population with 15.3 percent living with diabetes. Furthermore, it is estimated that about 15% of seven million people with diabetes mellitus in Germany suffer from Diabetic Foot Syndrome (DFS). Alarmingly, studies reveal that almost 50% of patients with Diabetic Foot Syndrome (DFS) have had major or minor amputations.

[qualityherb]

Naringin Extract – Top 10 Benefits a Person Can Have From It

Naringin Extract is considered a water-soluble flavonoid present in citrus. Albert Szent-Gyorgi first discovered it. These are colored pigments in fruits and plants. They are also known as a type of flavonoid, mostly in the glycoside form. Naringin extract is an orange-colored, acidic substance that can be found in grapefruit. It has been known to have the following benefits:

1. Inhibits Cancer Cell Growth –

Naringin is regarded as a natural chemotherapeutic agent that can inhibit the proliferation of various types of cancers. It can inhibit cancer cells from turning malignant and begins to act against them by preventing growth and cell division. While helping prevent cancer, it also serves as an antioxidant that helps fight free radicals responsible for causing cancerous changes in cells.

The naringin extract can act as an antioxidant. This means it can protect against cell damage from free radicals that are known to cause cancerous diseases. So those who want to avoid this kind of disease must consider taking a supplement of naringin extract.

2. Relieve Respiratory Infections or Colds –

It has the power to help relieve the symptoms of the common cold or respiratory infection. It contains bioflavonoids with vitamin A and can also support the immune system. Since it is known to help with immunity, it can help remove the virus and bacteria causing respiratory infections.

3. Helps Control Blood Sugar –

It is also known as the blood sugar regulator or blood glucose modulator. Another benefit of naringin extract is its ability to effectively modulate and control blood glucose levels which benefits those with diabetes.

It also helps stabilize blood sugar levels in cases of hypoglycemia or hyperglycemia. In addition, it helps by controlling the secretion of insulin and glucagon by the pancreas. Thus making use of this extract can provide benefits to people suffering from diabetes mellitus type 2.

4. Helps in Managing Metabolic Syndrome –

Metabolic syndrome is a medical condition that combines obesity with other medical conditions, such as high blood sugar, high blood pressure, and abnormal cholesterol. The naringin extract can help in managing metabolic syndrome since it contains flavonoids.

5. Helps to Slow Down the Aging Process –

Aside from helping manage diseases, naringin also can slow down a person’s aging process by reducing wrinkles and other signs in the skin, like dryness and discoloration. It will aid in treating age-related macular degeneration because it contains luteolin that can help protect against UVB rays.

6. Acts as a Good Antioxidant –

An antioxidant is a type of nutrient that helps protect the user’s body from free radicals that are known to cause cell damage. It is due to its ability to fight oxidative stress. Oxidative stress is reactive oxygen species damage, a process wherein molecules in the body are. Oxidative stress can also lead to health complications like cancer and heart disease. People who want these conditions out of their lives must consider taking naringin extract as a supplement.

7. Prevents Stomach Damage –

It can also help protect the stomach from ulcers, gastritis, and other chronic conditions. It acts as a good antioxidant, and this is because it contains flavonoids that can help fight free radicals in the body. Free radicals have been known to cause cell damage, and in turn, they can lead to stomach illnesses like gastritis and ulcers.

8. Improves Bowel Movement –

It also can help improve bowel movement by promoting water absorption in the small intestines. This helps speed up bowel movement while keeping bowels clean by flushing out unwanted matter that is present inside the intestines or colon.

9. Improves Bone Strength –

Its anti-inflammatory effects can also help the body in the production of collagen, which is a protein that helps strengthen bones and cartilage. This is especially helpful for those who are at risk of osteoporosis.

10. Increases Blood Circulation –

Naringin extract can also increase blood flow as it contains flavonoid that exhibits vasodilatation properties. Vasodilatation means to widen the blood vessels by causing more blood to flow through them when higher amounts of adrenaline or epinephrine are circulating in the body.

Naringin Extract

[richardmedisys]

Medical billing and coding are critical components of the healthcare industry, ensuring that healthcare providers are reimbursed for their services accurately and efficiently. For those specializing in internal medicine, understanding the basics of internal medicine billing is essential. This comprehensive guide will discuss the basics of the internal medicine billing and coding process, including common codes, payer requirements, and tips for maximizing reimbursements.

An Overview of Internal Medicine Billing and Coding Internal medicine is a medical specialty that deals with the prevention, diagnosis, and treatment of adult diseases. Billing and coding for internal medicine services involve several steps to ensure that healthcare providers receive proper compensation for their services.

Patient Registration and Insurance Verification: The billing process begins with patient registration. Accurate patient information is crucial, as it forms the basis for insurance verification. Insurance verification is essential to determine the patient’s coverage, co-pays, deductibles, and any pre-authorization requirements. Incorrect patient information can lead to claim denials. Code Selection: The next step is selecting appropriate Current Procedural Terminology (CPT) and International Classification of Diseases (ICD-10) codes. CPT codes describe the medical services provided, while ICD-10 codes represent the diagnosis or reason for the services. Claim Submission: Once the services are provided, the healthcare provider compiles the CPT and ICD-10 codes, along with patient and provider information, to create a claim. Claims are then submitted to the appropriate payer, which may be an insurance company, Medicare, or Medicaid. Claims can be submitted electronically or on paper. Payment and Denials: Payers review claims for accuracy and compliance with their guidelines. If the claim is approved, the healthcare provider receives payment. If the claim is denied, the provider must investigate the reason for denial and resubmit the claim if necessary. Common Billing and Coding Errors Billing and coding errors can lead to claim denials, delayed payments, and potential legal issues. Common mistakes include:

Upcoding or Downcoding: Using codes that do not accurately reflect the services provided can lead to fraud allegations. Unbundling: Separating services that should be billed together can result in claim denials. Failure to Document Medical Necessity: Insufficient documentation can lead to claims being denied due to lack of medical necessity. Coding for Non-Covered Services: Billing for services that are not covered by the patient’s insurance can result in claim denials and patient disputes. Common Internal Medicine CPT and ICD-10 Codes CPT and ICD-10 codes are essential for internal medicine billing. Below is a list of common codes organized by type of service:

E/M (Evaluation and Management) Services CPT Code 99213: Office or other outpatient visits for the evaluation and management of an established patient. ICD-10 Code Z00.00: Encounter for general adult medical examination without abnormal findings.

Preventive Services CPT Code 99396: Periodic comprehensive preventive medicine re-evaluation and management of an individual including an age and gender-appropriate history. ICD-10 Code Z13.3: Encounter for screening for mental health and behavioral disorders.

Chronic Disease Management CPT Code 99490: Chronic care management services, at least 20 minutes of clinical staff time per month. ICD-10 Code E11.9: Type 2 diabetes mellitus without complications.

Vaccinations CPT Code 90471: Immunization administration (includes percutaneous, intradermal, subcutaneous, or intramuscular injections) for a single vaccine. ICD-10 Code Z23: Encounter for immunization.

Tips for Avoiding Denials and Improving Reimbursement To enhance the internal medicine billing process and maximize reimbursements, consider the following tips:

Stay Informed: Keep up with the latest changes in CPT and ICD-10 codes, as well as payer policies. Accurate Documentation: Ensure comprehensive and accurate documentation that supports the medical necessity of services. Coding Compliance: Code services correctly, avoiding upcoding or downcoding. Regular Audits: Conduct regular internal audits to identify and rectify billing and coding errors. Communication: Maintain open communication with patients to ensure they understand their financial responsibilities. Staff Training: Invest in ongoing training for billing and coding staff to stay updated on industry changes. Appeal Denials: If a claim is denied, investigate the reason and, if necessary, appeal the decision with additional documentation. In conclusion, internal medicine billing and coding is a complex and critical aspect of healthcare operations. Accurate coding, compliance with payer requirements, and a well-structured billing process are essential for healthcare providers to receive proper reimbursement for their services. Staying informed, adhering to coding guidelines, and conducting regular audits can help improve accuracy, reduce denials, and ultimately enhance the financial health of internal medicine practices.

Partner with Medisys Data Solutions (MDS) for Superior Internal Medicine Billing When it comes to internal medicine billing, partnering with a trusted and experienced medical billing company is essential for the success of your practice. Medisys Data Solutions (MDS) stands out as the ideal partner for internal medicine billing for several compelling reasons. With our specialized expertise, precision in coding, compliance assurance, and commitment to enhancing revenue collection, we offer a comprehensive solution to optimize your billing operations. Join hands with us, and experience the benefits of a seamless, efficient, and cost-effective billing process that enhances your practice’s financial success. To learn more about our internal medicine billing services, contact at 888-720-8884 / info@medisysdata.com

[medvantagesolution]

Unmasking the Global Diabetes Epidemic: Understanding the dangers of “The Sweet Tooth"

EPIDEMIOLOGY OF DIABETES MELLITUS

Diabetes mellitus is a clinical syndrome with many causes, which is characterized by the presence of hyperglycemia (mellitus being Latin for ‘sweet’). Type 2 diabetes accounts for around 90% of cases, while type 1 diabetes accounts for most of the remainder. All types of diabetes is consequences of relatively or absolute insulin deficiency. Therefore, a Fellowship in Diabetes Mellitus is considered one of the most relevant fellowships around the world.

Together both the diabetes type 1 and type 2 are holding similar hyperglycemic complications but their etiology and pathophysiology are different. 

In type 1 diabetes, there is an absolute deficiency of insulin because of an immune-mediated destruction of insulin-producing β cells in the pancreatic islets of Langerhans. 

Contrast, in type 2 diabetes, concentrations of circulating insulin are typically elevated, but there is a relative deficiency of insulin because there is reduced sensitivity to insulin in peripheral tissues (because of obesity) and the β cells cannot make ample insulin to overcome this ‘insulin resistance’.

PREVALENCE AND DEATH RATE

Diabetes carries a heavy personal burden for those affected as well as high financial costs to health-care systems and society at large scale. 

In year 2017, diabetes causes 4 Million death globally and healthcare expenditure of diabetes was calculated globally around to be 60,51,51,16,500 Indian rupees or 10% of total healthcare expenditure.

The prevalence of diabetes is rising. Globally, it is estimated that 463 million people had diabetes in 2019 (9.3% of the world adult population), approximately 90% with type 2 diabetes. This figure is expected to reach700 million by 2045.

Prevalence is highest in middle eastern and low eastern parts of Africa and varying around the world. According to ethnicity and environmental factors (obesity, diet, low - habitual physical activity, urbanisation and economic development).

A pronounced rise in the prevalence of type 2 diabetes occurs in migrant populations from low-income to industrialized countries. In many high-income countries, type 2 diabetes is no longer rare in children and adolescents, particularly in people of South Asian countries because of these countries, increased survival is a factor underlying rising prevalence.

Type 1 diabetes is also subject to geographical variation and is generally more prevalent in countries closer to the polar regions. Finland for instance, has the highest rate of type 1 diagnosis per year at >60 per 100 000 of the population, whereas in China and Venezuela the incidence is only 0.1 per 100 000. The incidence of type 1 diabetes is also increasing: between 1989 and 2013, 3.4 % more children were diagnosed worldwide each year. Type 1 diabetes is more common inpeople of European descent than in other ethnic groups and, for reasons that are not understood, more people are diagnosed in the winter months more as compare to others.

MICRO AND MACRO VASCULAR COMPLICATION

Microvascular complications:

In Eyes leads to Retinopathy, Cataract ultimately to glaucoma. 

In Kidneys due to high blood glucose leads to high blood pressure and affecting nephrons leading to nephropathy. 

In Nerves hyperglycemia damages peripheral nerves system this will results in pain and numbness. Feet wounds will go undetected and will left untreated ultimately leading to gangrene.

Macrovascular complications:

In Brain there will be increased risk of stroke and cerebrovascular disease including transient ischemic attacks, cognitive impairment etc. 

In Heart due to high blood pressure and insulin resistance there is increased risk of heart-attacks and coronary heart disease. 

In Extremities peripheral narrowing of blood vessels will leads to peripheral neuropathy hands and feet wounds are likely to heal slowly and will lead to certain complications like gangrene and limb amputations.

Join the Medvantage Fellowship in Diabetes Mellitus to get a deeper and more precise understanding of diabetes and it's compollications.

[ben1d]

The Top 10 Most Dangerous Diseases in Cats: What You Need to Know

Cats are beloved members of our families, and their health is of paramount importance. While cats can be resilient, they are not immune to diseases that can be life-threatening. In this unique and brief guide, we will explore the top 10 most dangerous diseases in cats, providing you with essential knowledge to recognize the signs and seek timely veterinary care.

1. Feline Immunodeficiency Virus (FIV)

FIV, often called feline AIDS, weakens a cat's immune system, making them vulnerable to various infections. It is primarily transmitted through bite wounds during fights with other infected cats.

2. Feline Leukemia Virus (FeLV)

FeLV is a contagious disease that affects a cat's immune system and can lead to various complications, including lymphoma and anemia. It is spread through close contact with infected cats.

3. Feline Infectious Peritonitis (FIP)

FIP is a severe viral disease with no known cure. It primarily affects the abdomen and can be fatal. Early detection is crucial for managing symptoms.

4. Feline Hypertrophic Cardiomyopathy (HCM)

HCM is the most common heart disease in cats. It leads to the thickening of the heart muscles and can result in heart failure or blood clots.

5. Chronic Kidney Disease (CKD)

CKD is common in older cats and occurs when the kidneys lose their ability to function correctly. Early diagnosis and proper management can extend a cat's lifespan.

6. Diabetes Mellitus

Cats can develop diabetes, which affects their ability to regulate blood sugar. It requires regular insulin treatment and dietary management.

7. Upper Respiratory Infections

These infections, caused by various viruses and bacteria, can lead to severe respiratory distress. Vaccination can prevent some of these diseases.

8. Panleukopenia (Feline Distemper)

Feline panleukopenia is a highly contagious and often fatal disease. It can cause severe dehydration and gastrointestinal issues.

9. Toxoplasmosis

Toxoplasmosis can affect both cats and humans. It is transmitted through the ingestion of infected prey or contaminated food or water.

10. Rabies

Rabies is a zoonotic disease that affects both cats and humans. It is transmitted through bites from infected animals. It is preventable through vaccination.

Conclusion

Awareness and early detection are crucial in the battle against these dangerous diseases in cats. Regular veterinary check-ups, vaccinations, and maintaining a safe and clean environment are essential in keeping your feline friend healthy. If you notice any signs of illness or behavior changes in your cat, seek immediate veterinary attention. By understanding these diseases, you can take proactive steps to protect your cat's health and provide them with the best care possible.